How Fermented Plant Foods and Their Byproducts May Help Control Blood Sugar by Changing Plant Compounds Through Gut Microbes

Kimchi is a lactic fermentation of Brassica vegetables in which heterofermentative Leuconostoc species typically dominate early and are followed by lactobacilli; these consortia commonly generate mannitol (via fructose reduction), lactic and acetic acids, EPS, and a range of peptides that reshape the chemical context of the vegetable matrix [12,17]. Contemporary overviews of kimchi microbiology and metabolite formation consistently highlight these endpoints—especially mannitol and organic acids—as hallmarks of plant-based lactic fermentations [13].

As a recent example, a serial co-fermentation using Leuconostoc citreum S5 and Lactiplantibacillus plantarum KS2020 yielded a GABA-enhanced kimchi beverage, with viable counts reaching approximately 9.11–9.42 log colony-forming unit (CFU)/mL on day 1 at 5% sucrose; mannitol synthesized by Leuconostoc was subsequently depleted as L. plantarum grew, illustrating strain-level cross-feeding within kimchi fermentations [51]. While GABA enrichment is analytically robust and often highlighted as a potential antidiabetic lever, direct evidence that kimchi-derived GABA per se improves glycemic control in humans is scarce and derives mainly from preclinical models or studies with isolated GABA rather than from kimchi intervention trials. In practice, organic acids, mannitol, and EPS produced during vegetable lactic fermentation have clearer proximate links to gastric emptying, enzyme inhibition, osmotic effects, and barrier/inflammatory signaling, and are more likely to underlie the modest but measurable glycemic and metabolic changes observed in kimchi studies described below.

Sauerkraut—a spontaneous lactic fermentation of cabbage—shares core LAB consortia with kimchi (for example, Leuconostoc and Lactiplantibacillus/Pediococcus) and accumulates lactic and acetic acids together with strain-dependent EPS and volatile esters. In artisanal sauerkraut from two producers, pH fell rapidly within the first week (from 5.7 ± 0.2 to 3.8 ± 0.1 in SK1; from 5.7 ± 0.3 to 4.0 ± 0.02 in SK2), while LAB counts rose from approximately 3.4–3.6 to approximately 5.7–8.1 log CFU/mL by day 7 and reached 6.4 ± 0.5 (SK1) and 8.2 ± 0.2 (SK2) log CFU/mL by day 35; community succession shifted from early Leuconostoc mesenteroides/pseudomesenteroides to later L. plantarum/paraplantarum, with 220 LAB isolates recovered overall. Proton Nuclear Magnetic Resonance (¹H-NMR) profiling highlighted lactic/acetic acids and small-molecule signatures, and brine exposure modulated cytokine responses (↑Tumor necrosis factor-alpha (TNF-α)/Interleukin (IL)-6 with ↑IL-10 at 24 h) in a Peripheral Blood Mononuclear Cells (PBMC)–Caco-2 co-culture, consistent with postbiotic-driven immunomodulation [52,53].

Clinically, in a dormitory-controlled randomized feeding trial, 100 healthy adults were assigned to low (15 g/day) or high (210 g/day) kimchi intake for seven days while receiving identical menus and maintaining habitual physical activity. Both groups showed significant decreases in fasting blood glucose, total cholesterol, and low-density lipoprotein (LDL)-cholesterol after seven days, with dose-dependent effects. Lipid-lowering responses were more pronounced among participants with baseline total cholesterol ≥ 190 mg/dL or LDL-cholesterol ≥ 130 mg/dL. The fall in fasting blood glucose was significantly greater with high vs. low intake (between-group p = 0.003), with mean changes of roughly −5.3 mg/dL and −2.0 mg/dL, respectively [54]. These changes are modest in absolute magnitude but suggest that fermented vegetables can favorably modulate short-term cardiometabolic risk markers under controlled dietary conditions.

In prediabetes, a randomized 8-week crossover feeding study (n = 21) compared fresh (1-day) vs. fermented (10-day) kimchi, separated by a 4-week washout. Both periods reduced body weight, body mass index, and waist circumference, but fermented kimchi additionally decreased insulin resistance and increased insulin sensitivity, with significant improvements in HOMA-IR and Quantitative Insulin Sensitivity Check Index (QUICKI) (reported p = 0.004 and p = 0.028, respectively). The proportion of participants with improved glucose tolerance was 33.3% during fermented-kimchi intake vs. 9.5% with fresh kimchi; systolic and diastolic blood pressure (BP) also fell during the fermented period [21].

Mechanistically, strains isolated from kimchi can attenuate starch digestion in vitro: L. plantarum LRCC5314 inhibited α-amylase and α-glucosidase activities by approximately 72.9% and approximately 51.2%, respectively, supporting a plausible pathway for blunting early postprandial glycemic excursions [55]. In overweight and obese adults, a randomized crossover study (n = 22; two 4-week periods separated by a 2-week washout) reported greater net reductions with fermented compared with fresh kimchi in fasting glucose, total cholesterol, percent body fat, and systolic and diastolic BP; fasting insulin also tended to decline after fermented kimchi [56].

Beyond kimchi, observational data on other fermented vegetables point in a similar direction. In a prospective cohort from China (n = 6640 analyzed; approximately 10-year follow-up), regular consumption of pickled vegetables was associated with a lower risk of incident diabetes in a dose-responsive fashion (0–0.5 kg/month: odds ratio (OR) 0.77, 95% confidence interval (CI) 0.63–0.94; >0.5 kg/month: OR 0.37, 95% CI 0.23–0.60), and fermented bean curd intake was likewise associated with reduced risk (OR 0.68, 95% CI 0.55–0.84) after multivariable adjustment [57]. Short-term high vs. low kimchi intake has also been linked with shifts in gut microbiota composition, including reductions in potentially pathogenic taxa and significant changes across dozens of species in the high-intake group [58].

Overall, kimchi exemplifies how plant-based lactic fermentation can yield metabolite signatures (mannitol, organic acids, EPS, bioactive peptides, and other postbiotic components) with mechanistic links to glycemic control and measurable signals in humans—from short-term reductions in fasting glycemia and atherogenic lipids in healthy adults to improved insulin sensitivity and glucose tolerance in prediabetes. At the same time, recipe composition (notably salt and co-ingredients), fermentation length, and starter strain selection vary widely and likely contribute to between-study heterogeneity and to the modest, context-dependent magnitude of effects, an issue revisited in. Section 7

Fermenting soy increases β-glucosidase activity and converts isoflavone glycosides into aglycones, while proteolysis liberates bioactive peptides—changes that can plausibly affect glycemic handling via intestinal incretin and systemic signaling pathways. Comparable fermentation-driven peptide release has also been reported in emerging fermented legume products beyond soy, with enrichment of short, bioactive sequences (including DPP-IV-inhibitory peptides) in chickpea-, lentil-, and mixed-legume matrices following controlled fermentation and hydrolysis [59]. These developments suggest that the glycemic-relevant mechanisms described for traditional soy ferments may extend to a broader class of plant-based fermented protein foods.

In humans, an open-label, parallel intervention in healthy women (n = 16) included a 7-day soy washout followed by 28 days of either steamed tempeh (100 g/day; n = 10) or soymilk (200 mL/day; n = 6). Fecal Quantitative Polymerase Chain Reaction (qPCR) showed significant microbiota shifts with tempeh: Akkermansia muciniphila increased approximately 37-fold by day 29 and Bifidobacterium rose approximately 1.5-fold, whereas both taxa decreased in the soymilk group. Although glycemic endpoints were not measured, the magnitude and direction of these changes are consistent with a gut-mediated route through which soy fermentation might influence glucose homeostasis [60].

Beyond microbiological remodeling, modified tempeh formulations have been tested for glycemic and microbiome endpoints in diabetic rodent models. In streptozotocin–nicotinamide diabetic rats fed for 4 weeks with diets where casein was partially replaced by standard tempeh (15% or 30% of protein) or by a lactic-acid-bacteria-acidified "modified tempeh" (15% or 30%), groups differed significantly in fasting serum glucose (p < 0.001). The modified product also altered the cecal short-chain fatty acid profile (acetate/propionate/butyrate, all p < 0.001), increased bacterial diversity, and shifted the Firmicutes/Bacteroidetes ratio upward relative to diabetic controls; compositionally, the modified tempeh had higher protein (19.85 ± 0.02% vs. 17.03 ± 0.02), fat (10.85 ± 0.06% vs. 9.27 ± 0.01), and dietary fiber (8.20 ± 0.19% vs. 5.92 ± 0.02) than regular tempeh, indicating a distinct nutrient and postbiotic matrix relevant to host metabolism [61].

A companion 30-day study using the same processing strategy reported that the modified tempeh contained a higher LAB load (9.99 ± 0.09 vs. 7.74 ± 0.07 log CFU; p < 0.001) and improved glycemic readouts, with significant pre–post differences in serum glucose and insulin overall and strong negative correlations between gut-microbiota diversity and both Δ glucose (r = −0.63; p < 0.001) and Δ insulin-resistance index (r = −0.54; p = 0.003), supporting a microbiome-linked route to glycemic control in this preclinical model [62].

For miso, population data in outpatients with T2D indicate sex-specific associations with glycemic control. Habitual miso consumption correlated with lower mean hemoglobin A1c (HbA1c) and reduced visit-to-visit variability among women after multivariable adjustment (e.g., β for average HbA1c approximately −0.25, p = 0.009; similar directions for standard deviation (SD) and coefficient of variation (CV)), with no association in men [63]. These findings suggest that, at least in women with T2D, fermented soy pastes may contribute modestly to improved glycemic stability within the broader dietary pattern.

In acute settings, a randomized crossover single-meal study in healthy adults testing a legume-based miso-type sauce did not alter postprandial glucose or insulin vs. control, despite increases in plasma antioxidant capacity and favorable short-term lipid signals—underscoring that compositional or antioxidant improvements in fermented products do not automatically translate into detectable acute glycemic effects in low-risk populations [64].

In a high-fat/high-sucrose mouse model, dietary miso suppressed diet-induced impairments in glucose handling: Both intraperitoneal glucose tolerance (iPGTT) and insulin tolerance (ITT) area-under-the-curve values were significantly lower vs. control (n = 6/group; p < 0.05). Miso feeding also improved muscle function (higher grip strength and soleus muscle mass) and reduced muscle inflammation, with downregulation of Tumor Necrosis Factor alpha (TNF-α) and Chemokine (C–C motif) ligand 2 (Ccl2) expression (p < 0.05). SCFAs increased across matrices—including feces, serum, skeletal muscle, and epididymal white adipose tissue—supporting a gut–muscle axis contribution to metabolic effects, although these remain preclinical findings [65].

In the same outpatient framework, a cross-sectional analysis (n = 300) stratified participants by urine-estimated salt intake and habitual miso consumption. Obesity prevalence was 77.8% in high-salt/no-miso (+/−), 40.2% in high-salt/with-miso (+/+), 26.0% in low-salt/with-miso (−/+), and 34.8% in low-salt/no-miso (−/−). Using the high-salt/no-miso group as reference, adjusted odds ratios were 0.07 (95% CI 0.02–0.26; p < 0.001) for (−/+), 0.14 (0.04–0.51; p = 0.003) for (+/+), and 0.16 (0.03–0.76; p = 0.022) for (−/−), suggesting that habitual miso consumption attenuated the salt–obesity association in this cohort [66]. While these data are observational and not specific to glycemia, they are consistent with broader metabolic benefits of fermented soy pastes in real-world dietary contexts.

Beyond microbiota signals, natto—a Bacillus-fermented soy food rich in viscous γ-PGA—has shown acute glycemic effects in randomized crossover meal tests. In healthy adults, a three-arm trial comparing white rice, low-γ-PGA natto, and high-γ-PGA natto found that the glucose IAUC_0–120 was approximately 20.1% lower with high-γ-PGA natto vs. white rice (p < 0.05), with early-phase (0–45 min) suppression vs. low-γ-PGA natto as well; insulin IAUCs showed timing differences consistent with a viscosity-mediated slowing of starch digestion [18]. A second randomized crossover study that quantified γ-PGA doses (approximately 58 mg vs. approximately 440 mg per 40 g) likewise reported lower early-phase glucose and insulin IAUCs with the high-γ-PGA natto [22]. Collectively, these acute data support postbiotic viscosity (γ-PGA) as a proximate mechanism for blunting postprandial excursions in humans.

Overall, the soy/legume ferment category illustrates how multiple levers—(i) isoflavone aglycone enrichment, (ii) peptide release (including DPP-IV-inhibitory sequences), (iii) microbiota remodeling, and (iv) viscosity-building postbiotics such as γ-PGA—can converge on glucose regulation. At the same time, effects on glycemic endpoints are more consistently documented for high-γ-PGA natto than for other soy/legume ferments, and human data outside acute meal tests remain limited. This heterogeneity motivates the more mechanistic treatment inandand the design recommendations in. Section 4 Section 5 Section 7

Kombucha comprises a symbiotic consortium of yeasts and acetic acid bacteria (AAB) that remodel tea polyphenols and generate organic acids and cellulosic exopolymers [14]. Metagenomic and physicochemical profiling of commercial products consistently identifies Komagataeibacter/Acetobacter with yeasts in a cellulose pellicle, together with low residual sugars (e.g., glucose approximately 1.87 g/L, sucrose approximately 1.11 g/L, fructose approximately 0.05 g/L) and high total phenolics (approximately 290 mg gallic acid equivalents (GAE)/100 mL), indicating extensive carbohydrate utilization and polyphenol remodeling [67].

Untargeted metabolomics using ultrahigh-resolution Fourier Transform Ion Cyclotron Resonance Mass Spectrometry (FT-ICR-MS) has mapped yeast–yeast and yeast–AAB cross-feeding in simplified kombucha consortia (Brettanomyces bruxellensis, Hanseniaspora valbyensis, Acetobacter indonesiensis), assigning 506 features to unique molecular formulas (307 retained after replicate filtering) and identifying 136 "core metabolites" spanning Carbon, Hydrogen, and Oxygen/Carbon, Hydrogen, Oxygen, and Nitrogen/Carbon, Hydrogen, Oxygen, and Sulfur (CHO/CHON/CHOS) families; yeast–yeast coculture selectively increased peptide and fatty-acid signatures, whereas yeast–bacterium coculture shifted profiles toward organic-acid derivatives consistent with ethanol and sugar-acid oxidation [19]. A complementary FT-ICR-MS time course across production phases showed that the open-vessel acidification phase (P1) drove release/formation of gluconic acid (an AAB marker) and gallic acid, increased molecular diversity (e.g., 310 masses at day-7 black-tea kombucha vs. 138 in sugared black tea), and lowered pH from approximately 6.9 to approximately 4.2 with total acidity rising to approximately 20–41 meq/L; during the closed-vessel carbonation phase (P2), signals indicated consumption/transformation of oleic acid, and cellulose (1,4-β-glucan) signatures appeared as an additional AAB biomarker, with black-tea matrices showing more extensive polyphenol remodeling than green tea under comparable conditions [68]. Production-focused work with kombucha consortia also highlights BC as a salient postbiotic, with culture-system parameters modulating pellicle biosynthesis and properties [69].

Polysaccharide-focused work with mushroom-based kombucha variants (Trametes versicolor, Lentinus edodes) has revealed complex polysaccharide/phenolic signatures and in vitro immunomodulation in PBMCs (reduced Th2 cytokines and IL-10 without cytotoxicity up to 500 μg/mL), adding mechanistic context to kombucha's postbiotic repertoire, although glycemic endpoints were not assessed [70].

In adults with T2D, a randomized, double-blind, crossover pilot (n = 12; 4-week periods with washout) reported that daily kombucha intake (approximately 240 mL/day) reduced fasting blood glucose from approximately 164 to 116 mg/dL by week 4 (p = 0.035), whereas a matched placebo decreased from approximately 162 to 141 mg/dL without statistical significance; reductions were larger among participants with baseline fasting glucose >130 mg/dL [71]. In healthy adults, an acute crossover meal study showed that consuming kombucha with a high-carbohydrate meal lowered both the glycemic index (GI) (to approximately 68) and the insulin index (to approximately 70) vs. control beverages (p = 0.041 for both), indicating attenuation of postprandial excursions [72]. These two studies together suggest that kombucha may exert detectable glycemic effects in the context of marked dysglycemia (T2D) or high-glycemic-load meals.

By contrast, an eight-week, parallel, RCT in free-living healthy adults deliberately maintained on a low-fiber, low-polyphenol "beige" Western diet assigned participants 2:1 to kombucha (n = 20 randomized; n = 16 analyzed) or control (n = 10; n = 8 analyzed). During the four-week intervention within this period, the kombucha group consumed one 16-oz bottle per day (two servings in total); clinic staff were blinded, while participants could not be. The primary endpoint was change in gut-microbiome composition; secondary endpoints included metabolic and inflammatory markers (e.g., IL-6, IL-10, C-reactive protein). Between-group differences in fasting glucose, fasting insulin, HOMA-IR, lipids, BP, and waist circumference were not significant. Within the kombucha group, fasting insulin and HOMA-IR increased over time (both p = 0.021), whereas the control group showed a decrease in high-density lipoprotein (HDL)-cholesterol (p = 0.042). Self-reported GI symptoms (diarrhea/bloating) were more frequent with kombucha (31.25% vs. 12.5%), and overall compliance was approximately 96%. Shotgun metagenomics nonetheless identified enrichment of Weizmannia coagulans and several SCFA-producing taxa in kombucha consumers. The trial was registered (NCT06484504) and industry-funded, and all participants remained on the beige-diet background throughout, underscoring how baseline diet and metabolic status may condition glycemic and microbiome responses to kombucha [73].

Longer-term data also differentiate kombucha based on tea type. In an 8-week pre–post intervention (n = 46; 23 normal-weight and 23 with obesity), daily black-tea kombucha (200 mL/day) was chemically profiled to contain 145 phenolic compounds (approximately 81% flavonoids, 19% phenolic acids). Microbiota shifts favored commensals, with increases in Akkermansiaceae and the butyrate-producer Subdoligranulum in the obesity group (p = 0.031), alongside reductions in obesity-associated genera (Ruminococcus and Dorea). Fungal diversity rose (↑Saccharomyces; ↓Exophiala, Rhodotorula), and Pichia/Dekkera emerged as biomarkers post-intervention. Although the design lacked a non-kombucha control and did not systematically assess glycemic endpoints, the directional changes support a microbiota signal under routine black-tea kombucha intake [74].

Over 10 weeks, an RCT during a calorie-restricted weight-loss program (control n = 29; kombucha n = 30) tested daily green-tea kombucha (200 mL/day). Between-group differences in intestinal permeability and fecal microbiota were not significant; however, the control group worsened on selected markers (e.g., lactulose:mannitol ratio 0.032 to 0.043, p = 0.01; fecal pH 7.30 to 7.07, p = 0.04), whereas the kombucha group reported better gastrointestinal symptoms and showed distinct post-intervention serum-metabolome features. Within-group SCFAs declined in both arms (e.g., fecal butyrate: control 10.193 to 8.674 µg/g, p = 0.02; kombucha 9.129 to 8.005 µg/g, p = 0.01). Taken alongside the black-tea pre–post study, these findings suggest that black- and green-tea kombuchas may exert partly distinct microbiota and metabolome signatures in humans, but robust, tea-type–specific effects on glycemic markers have yet to be demonstrated [75].

In diet-induced obese mice with Non-alcoholic fatty liver disease (NAFLD) features, kombucha supplementation improved oral glucose tolerance and reduced fasting hyperinsulinemia; in the liver it lowered citrate synthase and phosphofructokinase-1 activities, downregulated bile acid–sensing receptors TGR5 and FXR at the gene-expression level, attenuated steatosis and collagen deposition, and restored acute insulin-induced protein kinase B (Akt) serine phosphorylation—indicating coordinated effects on hepatic carbohydrate and bile acid metabolism with histologic improvement [76]. A complementary high-fat, high-fructose rat model showed that 10 weeks of green- or black-tea kombucha with the obesogenic diet improved glucose metabolism, reduced circulating triglycerides and adiposity, and reversed liver steatosis while mitigating oxidative stress and inflammatory read-outs [77]. These mechanistic insights are currently confined to preclinical models and inform hypotheses about bile-acid and redox signaling (FXR/TGR5, AMPK/Nrf2) that require further testing in humans (Section 5).

Overall, kombucha emerges as a tea-based ferment with a Komagataeibacter–yeast core and an organic-acid/phenolic/cellulosic postbiotic repertoire. Human data suggest glycemic benefits in adults with T2D and during high-glycemic-load meals, but neutral or even adverse metabolic signals in some healthy cohorts. Comparative data on black-vs. green-tea kombucha in humans are still limited and indirect: Black-tea kombucha has mainly been linked to microbiota shifts in pre–post designs, whereas green-tea kombucha has been studied within hypocaloric diets with modest or null effects on gut permeability and composition. Across studies, a persistent limitation is the lack of standardized dosing (volume, fermentation time), organic-acid and ethanol profiling, and quantification of key polyphenols and postbiotic polymers, which hampers comparisons and attribution of effects. Taken together, current evidence indicates that kombucha's metabolic impact is context dependent and shaped by dose (approximately 240–330 mL/day), fermentation chemistry (including BC and organic-acid output), tea type, and background diet/metabolic status [78].

Water kefir is a sucrose-based fermentation in which translucent kefir grains act as living exopolysaccharide biofilms that host LAB, AAB, and yeasts; grain composition and metabolite output vary with substrate, mineral content, and temperature across producers and batches [15]. Detailed structural analysis of water kefir EPS shows that the insoluble grain polymers are predominantly dextran with an α-(1→6) backbone and O-3 branching, containing a higher proportion of 1,3-linked glucose units than the soluble fraction, whereas the beverage contains structurally distinct EPS—features consistent with contributions from multiple bacterial producers [20].

In practice, dextran synthesis by dextransucrase-positive Liquorilactobacillus hilgardii and related taxa scaffolds grain formation and growth. Time-resolved work tracking a 192 h fermentation showed that sucrose was completely consumed by 24 h, coinciding with the main burst of grain polysaccharide production; ethanol and lactic acid were the dominant metabolites, whereas glycerol, acetic acid, and mannitol accrued at lower levels, with most metabolite formation occurring within the first 72 h as pH fell from approximately 4.26 to approximately 3.45. The grain-associated microbiota comprised Lactobacillus casei/paracasei, L. harbinensis, L. hilgardii, Bifidobacterium psychraerophilum/crudilactis, Saccharomyces cerevisiae, and B. bruxellensis, alongside a volatile profile dominated by ethyl acetate, isoamyl acetate, ethyl hexanoate, ethyl octanoate, and ethyl decanoate [79]. Complementarily, shotgun metagenomics at 24 and 72 h (7.1% sucrose; 17.6% fig extract; 21 °C) identified L. hilgardii, L. harbinensis, L. nagelii, L. paracasei, a Lactobacillus hordei/mali–like species, Bifidobacterium aquikefiri, and the yeasts S. cerevisiae and B. bruxellensis, and uncovered a novel Oenococcus (Candidatus Oenococcus aquikefiri). Functional binning linked mannitol-from-fructose production to L. hilgardii, Candidatus O. aquikefiri, and B. aquikefiri, assigned dextransucrase genes to L. hilgardii, L. hordei/mali, and Candidatus O. aquikefiri, and highlighted cross-feeding (e.g., amino acid/cofactor supply) within the consortium [80].

Typical water-kefir fermentations yield lactic and acetic acids, carbon dioxide, trace ethanol, glycerol, and mannitol; the community structure and metabolite output vary with grain provenance, substrate (sugars and fruit additives), mineral content, and temperature across producers and batches [15,81,82]. In flavored systems, physicochemical and sensory trajectories—including pH and titratable acidity, residual sugars/ethanol, organic acids, volatile esters, color, and consumer liking—diverge by matrix and processing, underscoring matrix-driven variability relevant to translation work [83].

In soymilk kefir, fermentation increases β-glucosidase activity and shifts the isoflavone pool toward aglycones. Across ten soybean cultivars, aglycone daidzein increased from 17.35 to 60.15 μg/g in unfermented soymilk to 23.79–91.03 μg/g after 24 h of kefir fermentation; glycitein was not detected post-fermentation, while malonyl and acetyl conjugates declined. In the Guixia 2 cultivar, the sum of individual aglycones reached 72.07 ± 0.53 μg/g with selected starters, whereas total isoflavones showed a small reduction overall [84]. In parallel models, fermenting soymilk with L. plantarum LP95 produced a sustained acidic, antioxidant-enriched matrix (pH 6.5 to 4.2 in 24 h; viable counts >7 log CFU/mL through 49 days at 4 °C) with higher Trolox-equivalent antioxidant capacity and lower Thiobarbituric acid-reactive substances (TBARS) during storage, illustrating a stable postbiotic milieu in plant-based substrates [85].

Mechanistically, water-kefir LAB (for example, L. hilgardii) synthesize dextran and other branched glucans that increase viscosity and may slow starch digestion [15,20]. In plant-milk kefir, fermentation with kefir cultures produces α-galactosidase and β-glucosidase that hydrolyze raffinose and stachyose (reported up to approximately 100% and approximately 92%, respectively) and convert isoflavone glycosides to aglycones [86]; recent overviews of plant-based kefir systems also document EPS outputs, enzyme activities, and amylase-inhibitory signals across plant matrices, reinforcing the mechanistic plausibility for early postprandial attenuation [87]. These matrix- and strain-level differences mirror the physicochemical/sensory variability captured in flavored water-kefir models [83] and motivate standardized characterization in future human trials.

Human trials directly testing non-dairy/plant-based kefir for glycemic endpoints remain limited. Evidence from broader kefir meta-analyses—dominated by dairy kefir—suggests reductions in fasting blood glucose (weighted mean difference (WMD) −10.28 mg/dL, 95% CI −16.53 to −4.02; p = 0.001) and insulin (WMD −2.87 μU/mL, 95% CI −3.96 to −1.78; p < 0.00001), with no significant change in HbA1c overall [88]. We include one dairy kefir RCT in T2D (8 weeks, 600 mL/day) as a mechanistic benchmark—reporting greater reductions in fasting glucose (p = 0.01 between groups) and HbA1c (p = 0.02 between groups)—while noting that milk-specific components and matrix properties limit direct extrapolation to plant-based kefirs [89].

In high-fat/high-fructose diet (HFFD) rats, kefir-fermented soy milk inhibited digestive enzymes in vitro (α-amylase half-maximal inhibitory concentration (IC50) approximately 52.7 μg/mL; pancreatic lipase IC50 approximately 39.4 μg/mL) and, in vivo, lowered fasting blood glucose (approximately −36% vs. HFFD control), reduced intestinal and pancreatic lipase activities by approximately 26–35%, improved the lipid profile (↓Total Cholesterol (TC), ↓LDL; ↑HDL), and mitigated hepatic and renal injury markers—supporting a functional, enzyme-targeted route for glycemic improvement in a preclinical model [32,90]. In streptozotocin–nicotinamide diabetic rats, a goat- and soy-milk kefir combination produced a greater fall in plasma glucose than goat-milk kefir alone, increased glutathione peroxidase activity, and improved islet morphology with β-cell counts approaching those of non-diabetic controls [91].

Overall, plant-based kefir provides a reproducible LAB/AAB/yeast consortium embedded in dextran-rich grains, generates organic acids and EPS with plausible glycemic relevance, and increases isoflavone aglycones in soy matrices. At the same time, human glycemic evidence specific to non-dairy kefir is sparse and largely indirect, relying on extrapolation from dairy kefir and preclinical plant-based models. This defines a tractable gap that we revisit inand in the recommendations for future trials. Section 7

Sourdough fermentation broadens the plant-based portfolio by pairing LAB and yeasts to acidify cereal and pulse doughs, degrade phytate, remodel starch–protein–fiber networks, and accumulate organic acids—changes that collectively tend to slow starch hydrolysis and attenuate postprandial glycemic excursions. Comparative product testing generally indicates that sourdough breads display lower estimated GI than comparable yeast-leavened breads of similar flour composition, consistent with matrix-driven glycemic attenuation [16].

Formulation can further potentiate these effects. In a randomized crossover clinical trial, jabuticaba-peel-enriched sourdough bread increased fiber from approximately 1.0 to 2.3–2.9 g/100 g, raised antioxidant capacity 1.35–3.53× and total reducing capacity 1.56–2.67× vs. control, and maintained a 7-day shelf-life. Postprandially, the control bread elicited a glycemic peak at 30 min that persisted to 45 min, whereas the jabuticaba-peel sourdough produced a less prominent peak at 45 min with a smoother decline to 180 min; serum antioxidant capacity also rose by 3 h, while satiety profiles were broadly similar, with slightly higher satiety and lower desire to eat at 60 min for the enriched sourdough [92]. This study illustrates how combining sourdough fermentation with polyphenol- and fiber-rich by-products can shape both glycemic and redox trajectories, but its findings are not directly generalizable to simpler white-flour sourdoughs.

At the ingredient level, red-bean sourdoughs fermented with single (Lactobacillus fermentum) or mixed starters (L. fermentum + Kluyveromyces marxianus)—with or without wheat bran—showed significant reductions in tannins, phytic acid, and trypsin inhibitors, and increases in total phenolics, flavonoids, gallic acid, and soluble fiber; mixed-starter systems delivered the largest shifts, consistent with enhanced β-glucosidase, feruloyl esterase, and phytase activities. Bread quality also improved (higher specific volume, lower crumb firmness, better sensory scores). In mice, diets incorporating mixed-starter red-bean-plus-bran sourdough decreased serum pro-inflammatory cytokines, improved the HDL/LDL ratio, and enhanced glucose tolerance and insulin sensitivity; gut-microbiota diversity increased, with higher Bifidobacterium abundance and greater SCFA production vs. controls and white-bread comparators, supporting a microbiota-linked route to metabolic benefit [93].

Preclinically, feeding two sourdough breads to streptozotocin–nicotinamide T2D rats for one month improved hyperglycemia and oral glucose tolerance, favorably shifted oxidative and inflammatory markers, lipids, and liver/kidney function, and enhanced cognitive performance. The sourdough bread richer in unsaturated fatty acids (approximately 79.33% of total fatty acids) outperformed the higher-saturated-fatty-acid loaf (approximately 16.08% saturated fatty acids). Mechanistically, hippocampal Brain-Derived Neurotrophic Factor (BDNF) and Nrf2 expressions increased, while hepatic glucose transporter 2 (GLUT2) and phosphoenolpyruvate carboxykinase (PEPCK) were down-regulated, consistent with improved glucose handling and neuroprotection in this animal model [94].

Across cereals and pulses, sourdough processes offer a controllable LAB–yeast ecology that, via acidification, phytate degradation, network remodeling, and strategic co-delivery of fiber and polyphenols, can reduce predicted or acute glycemic impact in humans and improve glycemic endpoints in rodents. However, recent structured and systematic reviews of sourdough breads and low-GI products produced with microbial fermentation underline that these benefits are highly heterogeneous and strongly conditioned by flour type (wholegrain vs. refined), particle size, fermentation protocol (traditional, long-fermented Type I vs. shorter, industrial Type II systems), dough hydration, and co-ingredients [25,34]. Randomized trials in adults at risk for T2D, for example, show that modifying wholegrain flour particle size within bread formulations can yield only small or neutral changes in postprandial glucose and insulin responses, highlighting that flour characteristics alone do not guarantee clinically meaningful glycemic improvements [95]. Mechanistic work comparing spontaneous sourdough and solid-state fermentation of whole wheat further demonstrates that different fermentation strategies markedly alter acidification dynamics, protein network structure, and phenolic/tannin profiles—matrix properties that are directly relevant to starch digestibility and thus to glycemic response [96]. A broader overview of microbe-enabled low-GI cereal and legume products similarly concludes that the magnitude of GI reduction depends not on "sourdough" labeling per se, but on a combination of flour selection, fermentation time–temperature, and formulation [97]. To enable comparability across styles and co-ingredients, future human trials should therefore report, at minimum, flour type and cultivar, fermentation time and temperature, dough pH and titratable acidity, organic-acid profiles, in vitro starch digestibility metrics, and standardized postprandial endpoints, and a clear specification of whether Type I or Type II sourdough systems are used.

Fermentation supplies a relatively well-defined enzymatic toolkit that remodels plant polyphenols. Microbial β-glucosidases hydrolyze O-glycosides (e.g., rutin → quercetin; naringin → naringenin), tannases cleave galloyl and depsidic bonds (liberating gallic acid), esterases de-esterify phenolic esters (e.g., chlorogenic → caffeic + quinic acids), and phenolic-acid decarboxylases convert hydroxycinnamates into vinyl derivatives (e.g., p-coumaric → 4-vinylphenol; ferulic → 4-vinylguaiacol). Contemporary syntheses consistently describe this pattern across vegetable-, soy-, and tea-based ferments, together with concomitant rises in total phenolics and in vitro radical-scavenging capacity [6].

As a primary quantitative example comes from the fermentation of sea-buckthorn leaves with a β-glucosidase-producing Eurotium amstelodami strain (BSX001): Rutin decreased from 4.61 ± 0.13 to 0.92 ± 0.05 mg/g dry weight, while total phenolics increased from 55.97 ± 1.72 to 100.16 ± 3.25 mg GAE/g dry weight; aglycones (quercetin, kaempferol, isorhamnetin) rose in parallel and 2,2-diphenyl-1-picrylhydrazyl/2,2′-azino-bis (3-ethylbenzothiazoline-6-sulfonic acid)/ferric reducing antioxidant power (DPPH/ABTS/FRAP) readouts improved, documenting enzyme-linked deglycosylation and enhanced redox activity rather than simple concentration effects [98].

Although most of these data derive from in vitro or matrix-focused studies, the pattern is mechanistically relevant for glycemic control: Aglycones and low-molecular-weight phenolics differ from their parent glycosides in absorption, tissue distribution, and signaling properties, and can interface with redox-inflammation pathways and incretin biology. In later sections we explore how these fermentation-driven changes in phenolic profiles may contribute—alongside organic acids and polymers—to improved insulin sensitivity and postprandial glycemic handling, while noting that direct human evidence linking specific enzymatic transformations to glycemic endpoints remains limited.

In soy matrices, kefir-style and related fermentation consistently shift the isoflavone pool toward aglycones via microbial β-glucosidases. In a ten-cultivar screen, soymilk fermented for 24 h increased aglycone daidzein from approximately 17.35–60.15 μg/g (unfermented) to approximately 23.79–91.03 μg/g, while malonyl/acetyl conjugates declined and glycitein frequently fell below detection—patterns that reflect targeted enzymatic remodeling rather than simple concentration effects, with magnitudes dependent on cultivar and starter choice [84]. This aglycone enrichment is mechanistically relevant because aglycones exhibit higher intestinal bioaccessibility and distinct signaling properties compared with their parent glycosides, offering plausible links to incretin biology, redox–inflammatory tone, and ultimately insulin sensitivity, even though direct glycemic readouts are seldom reported in these analytical studies.

In a complementary plant-milk model, fermenting soymilk with L. plantarum LP95 yielded a refrigerated beverage that maintained viable counts >7 log CFU/mL over extended storage, displayed higher Trolox-equivalent antioxidant capacity, and exhibited lower lipid peroxidation vs. unfermented control [85]. Together with the isoflavone data, these findings support a stable, fermentation-derived postbiotic milieu in soy-based drinks that can sustain aglycone exposure and enhanced antioxidant capacity throughout shelf-life. At present, most of this evidence is matrix- and mechanism-focused; in subsequent sections we explore how similar deglycosylation patterns, when integrated with viscosity-building polymers and organic acids in whole meals, may contribute to the modest, context-dependent glycemic effects observed in human trials of fermented soy foods.

In kombucha and related tea ferments, microbial tannase and esterases liberate gallic acid from gallated catechins, while yeast–AAB cross-feeding oxidizes sugars and ethanol to organic acids such as acetic, gluconic, and lactic acids. Untargeted FT-ICR-MS in simplified consortia (e.g., B. bruxellensis, H. valbyensis, A. indonesiensis) has mapped these trajectories and the expansion of molecular diversity during acidification, with signatures of gluconic and gallic acids consistent with tannase activity and AAB-driven sugar-acid oxidation (as detailed in Section 3.1.3) [19]. Metagenomic and physicochemical profiling of commercial kombuchas corroborates a Komagataeibacter/Acetobacter–yeast core with low residual sugars and high total phenolics, indicating extensive substrate turnover and polyphenol remodeling [67]. Under comparable conditions, black-tea matrices tend to show more extensive polyphenol transformation than green tea, suggesting that tea type modulates the balance between catechin degradation, phenolic-acid release, and organic-acid accumulation.

Process-oriented studies reinforce and extend this biochemical framework. In a metagenomic–organoleptic evaluation substituting conventional black-tea extract with recycled plant substrates, Selvaraj and colleagues characterized both the Symbiotic Culture of Bacteria and Yeast (SCOBY) and the beverage: Komagataeibacter/Acetobacter cores with yeast partners were consistently present; fermentation reduced pH and increased titratable acidity, while total phenolics and antioxidant readouts (e.g., DPPH/ABTS) rose in parallel with substrate turnover [99]. Importantly, hedonic scores were maintained across formulations despite shifts in substrate and metabolite profiles, indicating that substantial biochemical remodeling—tannase-mediated release of phenolic acids and altered organic-acid profiles—can occur without compromising sensory acceptance.

Matrix and storage conditions further shape the organic-acid and phenolic landscape. In a soursop kombucha model, response-surface optimization highlighted 25 °C and 14 days as a suitable fermentation window; subsequent storage experiments showed that antioxidant activity peaked at 14 days at 25 °C under light, whereas total phenolics were highest at 7 days at 4 °C in the dark. Sugars declined over storage, ethanol dropped markedly, and organic acids (e.g., acetic, gluconic, malic) varied by condition [100]. When kombucha was spray-dried and encapsulated in gum arabic, retention of organic acids and antioxidant and antibacterial activities during storage was superior to that of the non-encapsulated beverage [101]. These findings illustrate how post-fermentation handling can substantially modify the apparent postbiotic profile, even when the starting fermentation is similar.

Pragmatically, these data argue that authors should report, at minimum, the substrate identity and tea type (black, green, mixed; with approximate polyphenol load, e.g., mg GAE/L), SCOBY/inoculum mass, fermentation time and temperature, and storage or encapsulation conditions, because these variables demonstrably shift sugar–acid trajectories, phenolic retention, antioxidant/antibacterial activity, and sensory readouts [100,101]. While most of these studies do not include direct glycemic endpoints, they define a mechanistic—tannase-mediated phenolic-acid release, catechin degradation, and organic-acid/cellulosic postbiotic production—that constrains how kombucha and other tea ferments might influence glucose metabolism in the human trials discussed in Section 3.1.3 and Section 6.

Vegetable lactic fermentations remodel Brassica/cabbage matrices via LAB-dominated successions and generate characteristic small molecules beyond simple preservation. In artisanal sauerkraut from two small-scale producers, pH dropped rapidly within the first week (from 5.7 ± 0.2 to 3.8 ± 0.1 in SK1 and 5.7 ± 0.3 to 4.0 ± 0.02 in SK2), while LAB counts increased from approximately 3.4–3.6 to approximately 5.7–8.1 log CFU/mL by day 7 and reached 6.4 ± 0.5 (SK1) and 8.2 ± 0.2 (SK2) log CFU/mL by day 35. Community succession proceeded from early L. mesenteroides/pseudomesenteroides to later L. plantarum/paraplantarum, with 220 LAB isolates recovered overall; ¹H-NMR fingerprints highlighted lactate and acetate among dominant low-molecular-weight features, and sauerkraut brines modulated cytokine responses (↑TNF-α/IL-6 with compensatory ↑IL-10 at 24 h) in a PBMC–Caco-2 co-culture—consistent with postbiotic-driven immunomodulation alongside organic-acid formation rather than a purely preservative effect [61].

In kimchi, sugar-alcohol and GABA pathways illustrate strain-level cross-feeding during lactic fermentation. A serial co-fermentation using L. citreum S5 followed by L. plantarum KS2020 produced a GABA-enhanced kimchi beverage, with viable counts of approximately 9.11–9.42 log CFU/mL on day 1 at 5% sucrose; mannitol synthesized by Leuconostoc was subsequently depleted as L. plantarum grew, documenting dynamic fructose-reduction → mannitol fluxes together with amino-acid decarboxylation in a plant matrix [51]. In parallel, starter selection of commercial kimchi manufacture using L. mesenteroides strains underscores mannitol-producing and EPS-forming phenotypes that co-define texture and metabolite outputs relevant to downstream function [53]. Mechanistically, kimchi-derived strains can also attenuate starch digestion in vitro: L. plantarum LRCC5314 inhibited α-amylase by approximately 72.9% and α-glucosidase by approximately 51.2%, providing a plausible interface between the fermentation-derived chemical milieu and early postprandial glycemic handling [55].

GABA production in kimchi is therefore best viewed as part of a broader postbiotic signature that includes organic acids, sugar alcohols, and EPS. While GABA has been linked to neuroendocrine and blood-pressure effects in preclinical models, its direct contribution to glycemic control in humans consuming kimchi remains poorly characterized and is often inferred indirectly from animal data or from studies using isolated GABA rather than food-based sources. In contrast, organic acids, mannitol, and EPS from vegetable ferments have clearer mechanistic links to gastric emptying, enzyme inhibition, osmotic effects, and barrier/inflammatory signaling, providing more immediate routes to explain the modest but measurable glycemic and metabolic signals observed in kimchi trials (). Section 3.1.1

Taken together, vegetable ferments such as sauerkraut and kimchi generate organic acids (lactate, acetate), sugar alcohols (mannitol), GABA, and strain-dependent EPS, superimposed on phenolic remodeling, with microbial succession, recipe, and starter choice determining the balance of these outputs. These low-molecular-weight acids, osmolytes, and biogenic amines form part of a postbiotic repertoire that can influence viscosity, barrier integrity, and host inflammatory tone—setting the biochemical context for the mechanistic pathways developed inand their translation to glycemic outcomes inand. Section 4.2 Section 5 Section 6

Across vegetables, soy, tea, and cereal/pulse doughs, a recurring analytical theme is that substrate, inoculum, and processing choices reshape both microbial consortia and the small-molecule landscape, which in turn conditions host-facing outcomes. Recent work on lactic acid bacteria-fermented cereal-based foods explicitly frames these low-molecular-weight acids, EPS, peptides, and cell-wall-derived fragments as a postbiotic repertoire, and links their antioxidant, anti-inflammatory, and enzyme-inhibitory activities to specific fermentation parameters and analytical markers, reinforcing the need to co-characterize chemistry and function in plant-based ferments [102]. Kombucha illustrates this dependency particularly well: Metagenomic and untargeted metabolomic work shows yeast–AAB cross-feeding with extensive substrate turnover, yet residual sugars, organic acids, and phenolics vary by tea type, inoculum mass, and fermentation/finishing steps. These data underscore the need to co-report substrate/tea specification, SCOBY mass, time–temperature, pH/titratable acidity, residual sugars (g/L), organic-acid profile (e.g., HPLC), ethanol %, and cellulose pellicle metrics alongside microbiome readouts when linking chemistry to physiology [19,67]. Production-focused studies likewise demonstrate that BC is a substantial, process-sensitive postbiotic in kombucha, arguing for its quantification when interpreting mechanistic and clinical findings [69].

Convergence across matrices is also evident at the consortia–metabolite–host interface. In preclinical work, kombucha-associated microbes reprogram host metabolic pathways and suppress lipid accumulation, aligning with the organic-acid/phenolic signatures observed in compositional studies and motivating paired host omics (transcriptome and metabolome) in future human trials [103]. Clinically, black- and green-tea kombucha interventions have reported shifts in gut microbiota composition, serum metabolome, and GI symptoms in adults with and without obesity [74,75]. However, systematic appraisals on kombucha trials consistently emphasize heterogeneity in dose, duration, product chemistry, and endpoints, making it difficult to integrate findings across studies [78,104]. Accordingly, cross-matrix studies should pair microbiome and host-omics endpoints with a minimal analytical panel—polyphenols (e.g., mg GAE/L), organic acids, residual sugars and ethanol, cellulose/pellicle metrics where applicable, viable counts, serving dose and frequency, and background diet—so that microbiota and metabolic outcomes can be meaningfully compared across fermented foods.

Downstream handling further modulates metabolite stability and bioactivity. Encapsulation or spray-drying with gum arabic can better preserve organic acids and antioxidant capacity during storage than the unencapsulated beverage, whereas storage time, temperature, and light materially shift sugar–acid profiles and functional readouts in fruit-tea kombuchas [83,99]. These observations generalize to other plant matrices and argue for explicit reporting of finishing, packaging, and storage conditions in the fermented products used for test meals and interventions, rather than assuming that freshly fermented and shelf-stored products are equivalent.

A second cross-matrix theme is postbiotic flux into the host. In a quantitative screen of foods and beverages, acetate emerged as the dominant SCFA; per serving, kombucha provided one of the highest oral acetate (approximately 1226 mg acetate per 330 mL bottle), alongside vinegars, which delivered several hundred to approximately 700–1018 mg acetate per tablespoon (e.g., apple cider vinegar approximately 1016 mg), placing them among the richest oral SCFA sources. In a pharmacokinetic study in healthy adults, a drink containing approximately 25.8 mmol acetate increased plasma acetate from approximately 121.3 to approximately 263.5 μmol/L at 60 min and raised acetate AUC (12,346 vs. 1292 μmol/L·min vs. control), while propionate AUC also rose despite minimal propionate in the drink—suggesting endogenous contributions [105]. Methodological notes from this work highlight lot-to-lot variability, potential analytical artifacts (e.g., tube contamination), and the need for 13C-labeled tracers and diet records, because matrix and co-ingested foods modulate absorption and systematic appearance. For fermented plant foods, this implies that postprandial glucose/insulin iAUCs should be paired with circulating SCFAs (ideally with isotopologues) and detailed reporting of beverage/food chemistry and background diet to distinguish exogenous SCFA delivery from microbiota-mediated endogenous production.

Quality and safety analytics intersect with mechanistic interpretation. Head-to-head testing of three kombucha cultures showed that concentrated fermented teas and derived vinegar exerted bactericidal activity comparable to reference antibiotics (approximately 1 mmol ampicillin against Escherichia coli or 0.01 mmol penicillin against Staphylococcus epidermidis); neutralizing the pH abolished these effects, indicating acid-driven killing [106]. Inoculation with macerated pellicles accelerated growth and acidification, and sucrose/glucose/fructose supported robust growth, whereas maltose/galactose/lactose performed poorly and were prone to mold contamination [106]. Separately, SCOBY-derived isolates degraded aflatoxin B1 in vitro in spiked media, with degradation dependent on the isolate and assay conditions, underscoring a potential biotransformation capacity within kombucha microbiota. Translational work should therefore specify starting contaminant loads, pH/time windows, and identify degradation products before inferring safety benefits [107]. More broadly, probiotic and bioprocess characterization frameworks recommend standardized strain-level annotation, viability/CFU reporting, and multi-omics-based function attribution [108], all of which are directly applicable to fermented-food trials that aim to link microbial biotransformation to glycemic endpoints.

At a minimum, plant-ferment studies should therefore report the following information: substrate identity/cultivar; inoculum source and mass (or strain-defined starters); fermentation time–temperature; pH and titratable acidity; residual sugars and organic acids (e.g., by HPLC); ethanol %; EPS/cellulose (g/L or pellicle mass/thickness where relevant); viable LAB/AAB/yeast counts; key phytochemical markers (e.g., isoflavone aglycones in soy; phenolic acids in tea; phytate reduction in cereals); finishing/packaging and storage conditions; background diet controls; and paired endpoints (glycemic iAUCs, incretins, circulating SCFAs, and microbiome/host-omics). This common grid—outlined conceptually in Table 1 and Table 2—will enable cleaner cross-matrix comparisons and more robust mechanistic attribution across vegetables, soy, tea, and cereal/pulse ferments. These proposed items are consistent with recent postbiotic-focused frameworks for LAB-fermented cereal foods, which likewise call for joint reporting of postbiotic profiles and bioactivity readouts in fermented plant matrices [102].

Across plant fermentations, polyphenol remodeling follows reproducible, enzyme-mediated routes. β-Glucosidases from LAB and yeasts cleave O-glycosidic bonds to liberate flavonoid aglycones (for example, rutin → quercetin; naringin → naringenin), increasing lipophilicity and intestinal bioaccessibility [109,110,111]. Operationally, food-grade β-glucosidases show pH optima around 4–6 and temperature optima near 30–40 °C, with certain wine-associated strains retaining activity under ethanol—conditions compatible with real food fermentations [110]. In soy models, fermentations with Lactobacillus/Bifidobacterium increase isoflavone aglycone fractions within 12–48 h, consistent with measurable β-glucosidase activity rather than simple concentration effects [111]. In leaf-based systems, controlled fungal–microbial fermentation yields quantitative shifts: Rutin decreases (approximately 4.61 → 0.92 mg/g dry weight) as quercetin/kaempferol rise, total phenolics nearly double (approximately 56 → 100 mg GAE/g DW) and DPPH/ABTS/FRAP readouts improve—direct evidence of enzyme-linked remodeling in a food-relevant matrix [112].

Food-grade esterases from LAB enact bona fide de-esterification of phenolic esters. A purified chlorogenate-active esterase from Lactobacillus helveticus efficiently hydrolyzes 5-caffeoylquinic acid (5-CQA, chlorogenic acid) to caffeic and quinic acids under mildly acidic, fermentation-relevant conditions and remains active in a real food matrix (defatted sunflower meal), where application lowered chlorogenic acids and prevented chlorogenic-acid-quinone (CGAQ)-driven greening—demonstrating in situ de-esterification rather than artefactual degradation [113]. Complementary surveys catalog microbial tannases and chlorogenate/phenolic esterases that cleave galloyl/depsidic and caffeoyl–quinic linkages and outline pH/temperature optima typical of fermented foods; structural work on the L. helveticus esterase delineates the catalytic pocket accommodating 5-CQA, providing a mechanistic basis for chlorogenic-acid → caffeic + quinic conversion in food systems [114]. Together, these lines of evidence establish the ester-to-acid trajectory as a canonical route that generates smaller, more bioaccessible phenolic acids with distinct biological profiles.

Phenolic-acid decarboxylases (PADs) then convert hydroxycinnamates into vinyl derivatives (for example, p-coumaric → 4-vinylphenol; ferulic → 4-vinylguaiacol), yielding smaller, more hydrophobic products with distinct sensory and biological footprints; cell-free PAD systems from food-grade microbes catalyze these reactions under mildly acidic conditions typical of vegetable and cereal ferments [115]. Collectively, the β-glucosidase/tannase–esterase/PAD triad provides a mechanistic scaffold for the glycoside-to-aglycone, ester-to-acid, and acid-to-vinyl-phenol trajectories that underpin the smaller-molecule, higher-bioaccessibility profiles repeatedly observed in fermented plant foods [84,113,115,116].

From a glycemic standpoint, these routes are best viewed as enabling mechanisms: They increase the pool of readily absorbable phenolics that can modulate redox status, endothelial and inflammatory signaling, and incretin pathways (seeand), but direct links to improved postprandial glycemia in humans remain largely inferential and are often supported by in vitro and animal models. In the following subsections, we connect these enzymatic patterns to specific matrices (soy/plant milks, tea, vegetables) and to downstream metabolites—including SCFAs and bile-acid-related products—that have more immediate proximity to glucose control. Section 5.2 Section 5.3

In soy matrices, fermentation consistently increases β-glucosidase activity and shifts the isoflavone pool toward aglycones. In a kefir-style soymilk model spanning ten soybean cultivars, aglycone enrichment was evident within 24 h: Daidzein rose from 17.35–60.15 μg/g (unfermented) to 23.79–91.03 μg/g after fermentation, while malonyl/acetyl conjugates declined and glycitein frequently became undetectable—demonstrating enzyme-linked remodeling rather than simple concentration effects [84]. In parallel, a plant-milk fermentation with L. plantarum LP95 produced a durable postbiotic matrix through cold storage (pH 6.5 → 4.2 in 24 h; viable counts > 7 log CFU/mL maintained for 49 days at 4 °C) with higher Trolox-equivalent antioxidant capacity and lower TBARS, supporting sustained aglycone exposure within a stable, acidified environment [85].

Beyond kefir grains, food-grade starter choices and analytics also govern the extent of deglycosylation. Standardized quantification in fermented plant milks reports net increases in genistein and daidzein with concomitant losses of malonyl forms, and highlights starter composition and cultivar as primary drivers of variability in 24–48 h processes [117].

A complementary ester route operates alongside β-glucosidases. A purified chlorogenate-active esterase from L. helveticus efficiently hydrolyzes 5-CQA into caffeic and quinic acids under mildly acidic, fermentation-relevant conditions and remains active in a real food matrix (defatted sunflower meal), where its application decreased chlorogenic acids and prevented CGAQ-driven greening—direct evidence of in situ de-esterification [118]. Surveys of food-grade phenolic-ester hydrolases (tannases; chlorogenate/phenolic esterases) detail cleavage of galloyl/depsidic and caffeoyl–quinic linkages and summarize fermentation-typical pH/temperature optima, explaining rises in free phenolic acids during plant-food fermentations [114,119].

Engineering strategies can further accelerate isoflavone remodeling. In a soy-beverage context, deploying yeasts with enhanced β-glucosidase capacity increased conversion of isoflavone glycosides to aglycones over conventional fermentations, reinforcing that enzyme dose and stability under acidic, low-temperature conditions are rate-limiting in practice [120].

Finally, legume fermentations illustrate a complementary peptide axis that may act alongside aglycone exposure in cardiometabolic profiles. In jack-bean tempeh, in vitro digestion across intestinal segments yielded absorbed fractions with high ACE-inhibitory activity—jejunum > duodenum > ileum—and peptide-rich hydrolysates showed stronger ACE inhibition than non-absorbed fractions (e.g., approximately 81% vs. approximately 72% inhibition in ileal models), identifying short proline- and hydrophobic-rich sequences as primary contributors [121]. While glycemic endpoints were not measured, these peptide effects co-travel with aglycone-rich matrices and are mechanistically compatible with postprandial modulation in human test meals.

Mechanistically, these aglycone-enriched profiles align with the β-glucosidase toolkit documented for food-grade lactic cultures and yeasts and complement esterase/tannase routes summarized in Section 4.2.1; together they yield smaller, more bioaccessible isoflavone forms within 12–48 h and create a postbiotic milieu (organic acids, EPS, viable LAB) that can plausibly modulate early postprandial glycemia via intestinal and incretin pathways [114,118,119].

In controlled kombucha prepared with a pure cultured "tea fungus," fermentation increased total polyphenols by approximately 77.14% and total flavonoids by approximately 69.23%. Quercetin and kaempferol rose by approximately 89.11% and approximately 70.32%, respectively; summed catechins increased by approximately 45.77%, and flavonol glycosides fell by approximately 38.98%. Simulated in vitro bioavailability increased by approximately 29.52% for total polyphenols and by more than sevenfold for flavonoids, together with higher antioxidant readouts (DPPH +43.81%, ABTS +35.08%). Correlation linked these gains positively to epigallocatechin (EGC), epicatechin (EC), epigallocatechin gallate (EGCG), epicatechin gallate (ECG), quercetin, and kaempferol, and negatively with kaempferol-3-glucoside. Mechanistic modeling supported a synergistic route in which organic acids disrupt leaf structure while tannase, polygalacturonidase, and fermentation-derived solvents (acids, alcohols, esters) drive catechin degallation and broader biotransformation [122].

Untargeted FT-ICR-MS mapping in simplified kombucha consortia (B. bruxellensis, H. valbyensis, A. indonesiensis) assigned 506 features to unique formulas (307 retained after replicate filtering) and identified 136 "core metabolites" set. During the open-vessel acidification phase, pH decline from approximately 6.9 to approximately 4.2 and total acidity rose to approximately 20–41 meq/L, with release/formation of gluconic and gallic acids and an expansion of molecular diversity (e.g., approximately 310 detectable masses at day 7 in black-tea kombucha vs. approximately 138 in sugared black tea). In the subsequent closed-vessel phase, oleic acid was consumed and 1,4-β-glucan signatures appeared, indicating cellulose pellicle formation [19].

Across fermented foods more broadly, network analyses show that modest shifts in community composition and co-adaptation histories predictably alter organic-acid and phenolic trajectories, helping explain inoculum-to-inoculum variation in kombucha chemistry [123].

Process comparisons further reinforce enzyme-driven catechin remodeling and its sensory consequences. When tea extracts were sequentially fermented with filamentous fungi (Trichoderma reesei or Aspergillus niger) followed by LAB, the fungal step hydrolyzed galloylated catechins (key bitterness/astringency contributors), whereas the LAB step decarboxylated subsets of organic and phenolic acids and metabolized saccharides while increasing alcohols and ketones. Sensory evaluation combined with multivariate analysis (Principal Component Analysis and Orthogonal Partial Least Squares-Discriminant Analysis (PCA/OPLS-DA)) clearly separated fermented beverages from their baselines, with floral/fruity gains tracking increases fermented in higher alcohol/ketone and reduced astringency consistent with catechin degallation [124]. In a complementary pickled-tea model, yeast-enhanced fermentation reshaped 198 volatiles and 115 non-volatiles compounds and, by sensory testing, reduced perceived bitterness, astringency, and sourness while enhancing floral notes; odor-activity and regression analyses implicated citronellol and linalool-oxide as contributors and highlighted medium-chain fatty acids as key drivers of the "acidic aroma" signature [125].

Analytically, rapid HPLC methods using silica monolithic columns can resolve eight catechins plus caffeine within approximately 7 min (LODs approximately 0.11–0.29 mg/L; LOQs approximately 0.33–0.87 mg/L; recoveries approximately 94–105%), enabling routine time-resolved quantification of catechin losses (EGCG/ECG) and gallic-acid gains during tea fermentations [126]. Baseline tea chemistry also conditions both sensory and chemical outcomes: In raw Pu-erh teas, taste-addition experiments identified theophylline and rutin as key positive modulators of sweet aftertaste (among 96 annotated taste components), underscoring why starting composition and mouth-residence chemistry matter when interpreting post-fermentation flavor and acceptability [127].

Together, these data delineate a coherent route in tea ferments: Fungal/yeast/lactic tannase and esterase hydrolyze galloyl linkages (e.g., EGCG/ECG → gallic acid + degallated catechins), acetic-acid bacteria expand organic-acid pools (acetic, gluconic) and synthesize cellulose pellicle, and process variables (tea type, inoculum history, fermentation/finishing conditions) shape the exact trajectories. These are primarily analytical and mechanistic observations, but they define specific, measurable catechin to-gallic-acid and sugar-to-organic-acid pathways that should be co-reported with human glycemic and microbiota outcomes when evaluating black- vs. green-tea kombucha and related ferments in clinical settings.

Fermented plant matrices frequently accumulate high-molar-mass microbial polymers—EPS, BC, and γ-PGA—that increase apparent viscosity, water binding, and gelation. These properties can slow starch–enzyme mass transfer and diffusional glucose outflow, providing a purely physical, meal-proximal route to blunting early postprandial glycemic excursions. Below we summarize the main polymer classes and the evidence linking their rheological behavior to digestion rate, noting where support comes from human meal tests (γ-PGA in natto) vs. rheology and in vitro digestion models (EPS/BC).

Finally, polymer–polymer and polymer–protein interactions can amplify viscosity and network strength. In kefir, for example, adding a polymerized whey–protein/pectin thickening system increases viscosity and densifies microstructure, with evidence of intermolecular aggregation between added pectin and in situ EPS [45]. In bread, sourdough and long-fermentation protocols modify the protein–starch matrix and in vitro starch digestibility in ways that track with measured textural and rheological changes [16].

From a translational perspective, these data collectively support a viscosity-based mechanism whereby microbial polymers—EPS, BC, and γ-PGA—can attenuate early postprandial glycemia. However, only γ-PGA in natto currently has direct human meal-test evidence. For kombucha and other EPS/BC-rich plant ferments, the mechanistic case rests on rheology and in vitro digestion models; future human studies should therefore co-report polymer metrics (yield, MW proxies, viscosity/flow curves) and starch-digestion endpoints (in vitro and postprandial) to strengthen enzyme → polymer → glycemic-response attribution.

Whereasaddressed polymer-driven viscosity, here we examine non-polymeric metabolites that act at the enzyme and epithelial levels. This subsection focuses on low-molecular-weight metabolites arising from fermentation (or delivered with fermented foods) and their proximal effects on starch digestion and postprandial glycemia. We emphasize (i) organic acids and SCFAs, (ii) gastric emptying and incretin signaling, and (iii) phenolic and indole derivatives generated by microbial remodeling, and how these link to enzyme inhibition, delivery kinetics, and incretin responses. Section 4.2.4

Taken together, human data support a modest, acute glycemia-lowering role for luminal organic acids delivered with foods (e.g., vinegars and, by extension, acidic ferments), whereas direct SCFA dosing mainly affects substrate use and energy expenditure with limited immediate impact on glucose. Gastric emptying and incretin signaling emerge as key proximal levers, but trials with sourdough-type products illustrate that changes in motility do not automatically translate into robust glycemic benefits. Fermentation-altered phenolics and derived postbiotics (including urolithins) provide complementary α-amylase/α-glucosidase and enterohepatic mechanisms, with supportive human readouts in non-fermented models and strong preclinical backing. We therefore recommend that future fermented-food trials pair enzyme assays on the actual matrices and targeted metabolomics with standardized postprandial sampling, explicitly distinguishing mechanisms supported by human data from those that remain primarily preclinical.

Building on Table 1 (polymer metrics), this subsection details non-polymeric analytes and design items required for transparent attribution. Here we outline analytical anchors and a minimal reporting set to connect enzyme-level mechanisms to metabolite dynamics and clinical endpoints. We specify what to quantify (analytes, matrices, time points), how to quantify it (HPLC/GC/LC–MS methods, derivatization, internal standards), and how to report trials (checklists) so that enzyme → metabolite → endpoint links are reproducible.

Reliable mechanism-to-endpoint inferences require validated assays on the actual matrices served (and, when relevant, plasma/urine) plus time-aligned sampling against postprandial curves. For fermented plant foods, core targets are as follows: (i) organic acids, residual sugars, and ethanol by HPLC/GC; (ii) phenolics (e.g., isoflavones, phenolic acids) by targeted LC–MS/MS; (iii) polymer surrogates that shape transport (BC mass/thickness; EPS yield and rheology); and (iv) plasma panels that can be synchronized to 0–120 min glycemic readouts. Key analytical anchors and reporting items are summarized in Table 2.

In dark/fermented-tea models, teabrownins increase circulating GLP-1 and improve postprandial control in mice; in enteroendocrine secretin tumor cell-1 (STC-1) cells, they stimulate GLP-1 release—consistent with GPCR-based signaling from fermentation-derived polyphenols [153]. Complementary mechanistic work identifies teadenol A, a fermented-tea metabolite, as a GPR120 agonist that augments GLP-1 secretion, supporting a receptor-level pathway from tea fermentation to incretin signaling [154].

These findings suggest that oxidized/dark-tea fermentations can generate metabolites with incretin-active potential. Nevertheless, human incretin readouts in fermented-tea or kombucha trials are essentially absent; most clinical work has focused on glucose, insulin, and lipids, without parallel GLP-1/GIP or DPP-IV measurement and with heterogeneous tea bases (black vs. green) and background diets (Section 3.1.3). Thus, GLP-1 stimulation by fermented teas should currently be viewed as a mechanistic hypothesis with strong preclinical support but limited human confirmation. Future trials should prioritize standardized active/total GLP-1 preanalytics [27] and integrate incretin endpoints into glycemic test meals.

Proteolysis during legume/soy fermentation liberates short, proline- and hydrophobic-rich peptides with DPP-IV inhibitory activity—one of the canonical antidiabetic mechanisms ascribed to fermented soybean foods (miso, doenjang, tempeh). Contemporary reviews synthesize this peptide route and its analytical hallmarks across soybean matrices, positioning fermented-soy products as plausible sources of GLP-1-preserving activity in mixed meals [155].

Quantitatively, food-grade plant protein hydrolysates bracket realistic potency ranges: In a head-to-head evaluation, soybean and pea protein hydrolysates showed DPP-IV IC₅₀ values of approximately 1.15 and approximately 1.33 mg/mL, respectively, with enriched proline and hydrophobic residues in active sequences—parameters that map well onto peptides released during fermentation [156].

Fermentation itself can heighten functional readouts and generate transport-competent peptides. In green lentils, 72 h solid-state fermentation with L. plantarum increased apical DPP-IV inhibition in a Caco-2 intestinal model to 37.3% (vs. unfermented), with detectable basolateral activity (7.9% inhibition at 500 mg/mL) and identification of peptide fractions capable of transepithelial passage—demonstrating both enhanced inhibition and intestinal permeability of fermentation-derived peptides [157].

Together, these data support a peptide-centric mechanism whereby legume/soy fermentations supply DPP-IV-inhibitory oligopeptides at physiologically relevant potencies. However, human evidence linking these peptides to incretin profiles is still missing; to our knowledge, no trial has yet co-measured plasma DPP-IV activity and active GLP-1 after fermented-soy meals with well-characterized peptide profiles. Bridging this gap—by integrating targeted peptidomics with incretin and glycemic endpoints—will be critical to validate this mechanism in vivo.

Strains isolated from fermented vegetables (kimchi and related lactic ferments) repeatedly show probiotic hallmarks—acid/bile tolerance and pathogen antagonism—together with enzyme-level effects relevant to glycemic control; across in vitro screens, Lactiplantibacillus/Lactobacillus isolates inhibit digestive carbohydrases (α-amylase/α-glucosidase) and dampen inflammatory readouts in epithelial/immune co-cultures, while extracts/fractions from vegetable ferments likewise display α-glucosidase inhibition in food-relevant models, consistent with fermentation-remodeled phenolics and small organic acids [167,168,169,170,171,172].

Across rodent models, soy ferments improve glucose handling and insulin resistance while attenuating hepatic injury. In HFD rats, daily oral administration of fermented soybean meal produced with Lactobacillus plantarum FPS2520 and Bacillus subtilis N1 for 6 weeks significantly lowered fasting glucose, fasting insulin, and HOMA-IR and reduced OGTT AUC vs. HFD controls; liver injury markers (AST/ALT) also fell, consistent with improved glycemic control and hepatic status under a fermented-soy background [173]. In HFD-fed mice, supplementation with cheonggukjang (a short-ripened fermented soybean paste) led to significantly lower fasting glucose and insulin than HFD controls and improved hepatic steatosis, indicating anti-obesogenic effects that extend to glycemic endpoints [174]. Mechanistically, the fermented-soy intervention in rats above used a defined two-stage fermentation (first B. subtilis, then L. plantarum), and authors discuss synergy between microbial metabolites and isoflavone remodeling, aligning with enzyme-level routes (e.g., DPP-IV/α-glucosidase inhibition) prioritized earlier in Section 5. Nonetheless, these benefits have been demonstrated under obesogenic, high-fat contexts and relatively high doses in rodents; human data on tempeh/miso/natto summarized in Section 6.2.2 generally show more modest effects on glycemic endpoints.

In diet-induced obese mice with NAFLD features, Xu et al. [175] reported that daily kombucha supplementation improved oral glucose tolerance (lower OGTT AUC), reduced fasting hyperinsulinemia, and ameliorated hepatic steatosis and collagen deposition. Mechanistically, kombucha normalized insulin signaling (restored insulin-stimulated Akt phosphorylation), down-modulated hepatic bile-acid receptor pathways (TGR5/FXR) and shifted gut microbiota toward health-associated taxa (e.g., enrichment of Akkermansia), aligning liver histology and signaling with better systemic glucose handling [175]. These findings echo earlier kombucha studies summarized above: Cardoso et al. [77] showed improvements in glucose metabolism and liver fat under a HFFD background, and Moreira et al. [76] reported better glucose tolerance with mitigation of hepatic steatosis—together consolidating kombucha's preclinical signal on glycemic control and liver health.

In streptozotocin–nicotinamide (STZ/NA) diabetic rats, a mixed goat–soy kefir increased endothelial NO bioavailability via Endothelial Nitric Oxide Synthase (eNOS) upregulation, together with anti-inflammatory signals—placing kefir matrices on a vascular–metabolic route [176]. In HFFD models, soy-milk kefir inhibited α-amylase/lipase in vitro and improved metabolic readouts in vivo, consistent with enzyme-level attenuation of postprandial excursions [32]. Complementing these data, a water-kefir grain-derived L. paracasei strain strengthened intestinal tight-junction markers and reshaped the gut microbiota in diabetic mice, aligning barrier repair with metabolic improvements—a barrier → metabolism route relevant to tibicos/water-kefir matrices [177]. As with kombucha, however, most of this evidence remains preclinical, and extrapolation to non-dairy kefirs consumed by humans should be made cautiously until dedicated trials are available.

Sourdough fermentation reorganizes the cereal starch–protein matrix and enriches dough with organic acids, EPS (including β-glucans and dextrans), phenolics, and peptides. Together, these changes modulate starch gelatinization, enzyme accessibility and colonic fermentability, making sourdough an archetype of "postbiotic" bakery matrices with potential for glycemic modulation. Recent syntheses highlight that sourdough can increase resistant starch (RS) and slowly digestible starch (SDS), lower RDS, and thereby reduce the glycemic impact of cereal products, though effects are highly context-dependent [23].

Overall, the sourdough preclinical literature supports a coherent chain of mechanisms: Acidification, organic-acid production, and EPS formation, restructuring of the starch–protein–fiber matrix, and liberation of peptides and phenolics can synergistically lower GI and improve lipid and inflammatory profiles. At the same time, the magnitude—and sometimes even the presence—of glycemic benefits is highly formulation-dependent, varying with flour type (refined vs. whole, gluten-free pseudo-cereals), sourdough process (Type I vs. II, defined vs. spontaneous starters, fresh vs. freeze-dried), fermentation time/temperature, and co-ingredients. This context dependence is crucial for interpreting human intervention trials and head-to-head comparisons inand, where ostensibly similar "sourdough" products may differ sharply in their capacity to translate these mechanistic advantages into clinically relevant improvements in postprandial glycemia. Section 6.2 Section 6.3

Human intervention data are still sparse for tea- and kefir-based ferments, but two kombucha trials and one kefir trial begin to outline their metabolic profile. In an acute randomized crossover GI study (n = 11), a standardized high-GI rice meal was consumed with soda water, diet soft drink, or an unpasteurized live kombucha; while GI and insulin index (II) were virtually identical with soda water and diet soft drink (GI approximately 84–86; II approximately 81–85), kombucha reduced both indices to approximately 68 and approximately 70, respectively (p = 0.041 vs. soda water), indicating a statistically significant attenuation of acute postprandial glucose and insulin responses in this small pilot [72]. Complementing this acute signal in healthy volunteers, Mendelson et al. [71] performed a double-blind randomized crossover pilot in adults with T2D (n = 12), assigning participants to 240 mL/day kombucha or a sensory-matched placebo for 4 weeks, with an 8-week washout. Kombucha lowered mean fasting blood glucose from 164 to 116 mg/dL over 4 weeks (p = 0.035 vs. baseline), whereas the placebo drink produced a more modest, non-significant reduction (162 to 141 mg/dL, p = 0.078), suggesting that daily kombucha may exert an adjunctive anti-hyperglycemic effect in T2D, albeit in a small, short-duration study. In contrast, evidence for kefir comes mainly from dairy-based products and is more equivocal for glycemic endpoints: In an 8-week parallel RCT in 80 adults with non-alcoholic fatty liver disease, Mohammadi et al. [186] compared a calorie-restricted diet alone vs. the same diet plus 500 mL/day milk kefir. Despite comprehensive assessment of fasting blood sugar, insulin, HOMA-IR, lipids, and inflammatory markers, there were no significant between-group differences in changes in fasting glucose, insulin, or insulin resistance; only HDL-cholesterol and fat-free mass increased significantly in the kefir arm relative to control. A recent meta-analysis of kefir interventions in adults nevertheless reports small but statistically significant pooled reductions in fasting blood glucose (approximately 8 mg/dL) and HOMA-IR, with no consistent effects on anthropometry or lipid profile, underscoring that any glycemic benefit is modest and context-dependent, and that virtually all current evidence derives from dairy kefir rather than plant-based or water kefir formulations.

Human data on fermented soy are still limited but converge on two main themes: (i) γ-PGA-rich natto as a viscosity-driven modulator of early postprandial glycemia, and (ii) miso- and tempeh-based low-GI foods that primarily affect lipids and oxidative stress, with modest or neutral effects on conventional glycemic endpoints.

In a pair of randomized crossover meal tests in healthy Japanese adults, white rice alone was compared, rice with low-γ-PGA natto, and rice with high-γ-PGA natto. In the pilot trial, high-γ-PGA natto reduced the 0–120 min glucose iAUC by approximately 20% vs. white rice, with significant attenuation of both glucose and insulin iAUC in the early phase (0–15, 0–30, and 0–45 min), while low-γ-PGA natto produced smaller, mostly non-significant effects [18]. In the subsequent trial focusing on early-phase dynamics, the high-γ-PGA natto again lowered glucose and insulin iAUC vs. low-γ-PGA natto within the first 30–45 min after meal loading, without major differences in later time points, reinforcing a viscosity-mediated slowing of glucose appearance rather than a strong effect on total glycemic exposure [22]. These studies provide proof-of-principle that highly viscous natto can selectively blunt early excursions in postprandial glucose and insulin, a pattern that may be particularly relevant for cardiovascular risk even in otherwise normoglycemic adults.

Building on this mechanistic signal, Papagianni et al. [64] developed a legume-based, carotenoid-enriched miso-type sauce and evaluated it acutely in a crossover RCT in young healthy volunteers (n = 14). A high-fat, high-carbohydrate rice meal with the functional miso-type sauce was compared with the same meal containing a non-fermented control sauce. The functional sauce did not significantly modify postprandial glucose, but increased plasma total antioxidant capacity (FRAP) at 3 h, attenuated the rise in triglycerides during the last 1.5 h, and lowered LDL-cholesterol and platelet aggregation vs. baseline, consistent with an oxidative-stress and lipid/platelet-targeted benefit rather than a primary glycemic effect. In a follow-up 30-day randomized crossover pilot in healthy adults (n = 10), the same group compared 20 g/day of the bifunctional miso-type sauce with an energy-matched legume-based control; fasting glucose remained unchanged, but the miso-type sauce slightly reduced triglycerides and increased plasma total antioxidant capacity, while both sauces increased LDL-cholesterol, with a smaller increment in the miso arm. Together, these trials suggest that miso-type ferments enriched with carotenoids may contribute more robustly to redox and lipid modulation than to fasting or postprandial glycemia per se [187].

Tempeh-based products appear mostly in the form of low-GI snack prototypes rather than long-term efficacy trials. In a GI study of "tempeh gembus" cookies, Manullang et al. [188] substituted wheat flour with 0, 25, and 50% tempeh gembus flour and measured glycemic responses in vivo alongside in vitro digestibility. Cookies with 50% tempeh flour had the lowest GI (approximately 47, low-GI range) and glycemic load (approximately 6.9 per serving), together with the highest dietary fiber (approximately 25% w/w) and reduced in vitro starch digestibility, supporting the design of tempeh-rich snacks that minimize postprandial glycemic load while providing ferment-derived fiber and protein. Although this study is small and primarily technological, it illustrates how incorporating tempeh flour into compound foods systematically reduces the GI and GL in humans, in line with in vitro reductions in starch digestibility.

Evidence in patients with T2D is even more limited and often focuses on lipids. In a 4-week RCT in Indonesian adults with T2D (n = 64), Fatmah [189] compared two low-GI high-fiber biscuits: a "caromma" biscuit based on modified cassava and koro sword beans, and a "temma" biscuit containing tempeh flour plus date jam. Both biscuits were consumed at 100 g/day. Fasting blood glucose decreased modestly in both groups (approximately 15–25 mg/dL), but changes did not reach statistical significance, whereas total cholesterol, LDL-cholesterol, and triglycerides fell significantly and to a similar extent in both arms, consistent with a high-fiber, low-GI effect in which the specific contribution of tempeh is difficult to isolate.

Finally, large-scale observational data provide complementary, albeit indirect, support for fermented soy within healthy dietary patterns. In a longitudinal cohort of >65,000 Korean adults followed for approximately 5 years, Park et al. [190] showed that an Asian-style balanced diet pattern—characterized in part by higher fermented soy intake and a favorable modified Healthy Eating Index—was associated with greater waist-circumference reduction and lower metabolic syndrome risk, independent of energy intake and polygenic risk scores for abdominal obesity. Although this design cannot attribute effects specifically to fermented soy, it situates natto, miso, and related ferments within a broader metabolic health-promoting dietary context that resonates with the more mechanistic γ-PGA natto and miso-type sauce trials.

Human trials with sourdough cereal products are dominated by acute and short-term crossover designs, and collectively point to modest, context-dependent effects on postprandial glycemia. In healthy adults, Chatonidi et al. [191] compared lactic-acid-rich sourdough bread with an otherwise similar yeast-leavened bread and found that sourdough slowed gastric emptying and reduced early postprandial glucose and C-peptide excursions (15–90 min) without altering total glycemic AUC or ad libitum energy intake at a subsequent meal. In a follow-up three-period crossover, the same group tested whole-meal yeast bread, sourdough bread, and a yeast–sourdough bread over three 2-week periods; despite small differences in satiety hormones (PYY, GLP-1, C-peptide), postprandial glucose profiles, gastric emptying, ad libitum energy intake and fecal microbiota composition were essentially comparable across breads [192]. Similarly, Dall'Asta et al. [193] reported no differences in 2 h glucose or insulin iAUC when 12 healthy subjects consumed seven isoglucidic breads differing in wheat genotype (evolutionary vs. modern) and leavening (yeast vs. sourdough). In overweight/obese adults, sourdough pasta did not differ from conventional pasta in acute glycemic or insulinemic responses, nor in OGTT responses after 5-day consumption, although sourdough accelerated gastric emptying and modestly altered fecal SCFA and mycobiome profiles [140]. A recent GI trial in 10 healthy adults showed that manipulating formulation (whole-meal flour, added intact cereals) and baking time of part-baked sourdough breads shifted GI values downward but remained within the medium–high GI range and did not systematically translate into higher satiety iAUC [194]. By contrast, in 12 individuals with T2D monitored with flash glucose sensors, sourdough bread and a functional low-sugar, low-GI bread prepared with "biocrystal" alkaline water produced significantly lower interstitial-glucose AUC₀–₂₄₀ min, smaller glucose rises at 60–180 min, and lower peak insulin than conventional yeast bread, despite matched carbohydrate loads [36]. Overall, current human data support small sourdough-related improvements in early-phase glycemic and insulinemic responses—particularly when organic acid content is high and/or in T2D—while total glycemic exposure (iAUC), fasting glycemia and longer-term insulin sensitivity remain largely unchanged in short-term trials.

Kimchi and related salt-fermented vegetables raise obvious concerns about sodium exposure, particularly when consumed daily in 100–200 g portions. However, epidemiologic and intervention data suggest a more nuanced picture. Cross-sectional and 12-year cohort analyses in Korean adults report that high kimchi intake (≥145–200 g/day) is not associated with higher hypertension prevalence or incident risk in the general population, with a possible exception of watery kimchi in obese men; authors hypothesize that high potassium, fiber, and vegetable content may partially offset sodium's pressor effect [197,198]. In spontaneously hypertensive rats, high-sodium kimchi further elevated BP, whereas low-sodium kimchi did not differ from control diet, supporting reformulation as a viable strategy [199]. A recent scoping review of kimchi trials concludes that short-term human interventions (typically 50–200 g/day for up to 12 weeks) do not worsen BP and, in some cases, modestly lower systolic/diastolic values when kimchi replaces other salted foods. For metabolic trials, this means that sodium content and potassium balance should be explicitly reported and, where possible, low-sodium and/or potassium-enriched formulations should be prioritized in individuals with hypertension or high cardiometabolic risk [56,58].

Ethanol is an underappreciated safety and regulatory issue for kombucha and other sugar-fermented beverages. Under controlled conditions, commercial kombucha typically contains <0.5% alcohol by volume (ABV), but surveys of retail products and home brews have repeatedly documented batches exceeding 0.5–1.0% ABV and, in some cases, reaching approximately 2–3% ABV over the shelf life due to continued fermentation [200]. Regulatory guidance in several jurisdictions now requires producers to monitor ABV over the stated shelf life, keep values below 0.5–1.0% depending on alcohol legislation, and clearly label alcohol content and refrigeration instructions [201]. Case reports and toxicology reviews describe rare but serious adverse events with improperly brewed, unregulated kombucha (lactic acidosis, hepatotoxicity, heavy-metal exposure), typically linked to home production rather than commercial beverages. The randomized pilot in T2D reporting improved fasting glycemia noted no serious adverse events over 4 weeks, but its small size and short duration preclude firm safety conclusions [71]. Future kombucha and similar beverage trials should routinely quantify ethanol and organic acids, report ABV in publications, and define exclusion criteria for children, pregnancy, and individuals with alcohol use disorders.

Overall, lactic-fermented plant foods show a favorable GI safety profile, with most RCTs reporting no serious adverse events and only mild, transient symptoms (bloating, gas, changes in stool frequency) when fermented products are introduced [24]. In the natto, miso-type sauce, sourdough, and kombucha trials discussed above, dropout due to GI intolerance was rare, and adverse events were comparable between fermented and control arms [22,64,140,193,202]. A recent systematic review of fermented-food interventions found that, across diverse matrices, fermented foods tend to improve bowel-movement frequency, stool consistency, and functional GI symptoms, with occasional increases in flatulence during the first weeks of consumption [24]. Nevertheless, gas-producing substrates (cabbage, wheat) combined with microbial fermentation can exacerbate bloating or pain in individuals with irritable bowel syndrome or small intestinal bacterial overgrowth; for such patients, slow titration of dose and careful matrix choice may be warranted [203]. From a reporting perspective, standardizing GI adverse-event capture (e.g., Rome IV-aligned symptom diaries) and including tolerability as a predefined secondary endpoint would materially strengthen the safety evidence base [204].

In summary, heterogeneity in dose, duration, matrix composition, and safety profiles complicates interpretation of glycemic signals from plant ferments. Where benefits are seen, they tend to arise from well-characterized, "high-intensity" ferments (e.g., high-γ-PGA natto, strongly acidified or low-GI sourdough, carefully brewed kombucha) and in participants with impaired glucose regulation. At the same time, sodium load from fermented vegetables and ethanol from kombucha remain important safety considerations, especially for vulnerable groups. These themes foreshadow the methodological and reporting gaps addressed inand point toward the need for multi-arm, dose-ranging trials with rigorous metabolite and safety characterization. Section 7