New findings on muscle fat and meat quality in chickens: roles of genes and diet

In Jingxing-yellow chickens, comparative transcriptome analysis revealed that the PPAR signaling pathway and the steroid biosynthesis pathway play important roles in the regulation of IMF deposition (Table 1). Genes associated with adipogenesis and lipogenesis, including adiponectin, C1Q, and collagen domain containing (ADIPOQ), cluster of differentiation 36 (CD36), FABP4, fatty acid binding protein 5 (FABP5), LPL, stearoyl-CoA desaturase (SCD), perilipin 1 (PLIN1), cell death-inducing DNA fragmentation factor-like effector C (CIDEC), and peroxisome proliferator activated receptor γ (PPARG), as well as genes related to steroid biosynthesis, including 24-dehydrocholesterol reductase (DHCR24), lanosterol synthase (LSS), methylsterol monooxygenase 1 (MSMO1), NAD(P)-dependent steroid dehydrogenase-like (NSDHL), and cholesterol 25-hydroxylase (CH25H), were shown to be associated with high TG content in breast muscles [39]. A GWAS analysis identified the solute carrier family 16 member 7 gene (SLC16A7) as a key candidate gene associated with muscle TG content. Subsequent experiments demonstrated that SLC16A7 promotes TG deposition in chicken myocytes by regulating de novo lipogenesis (DNL) [40]. In Guizhou-yellow chickens, a local breed in China, comparative transcriptome analysis showed that pathways such as focal adhesion, ECM‒receptor interactions, cell adhesion molecules, actin cytoskeleton regulation, and the PPAR signaling pathway may be involved in IMF deposition in the breast. Genes such as calpain 2 (CAPN2), collagen type I alpha 1 chain (COL1A1), collagen type I alpha 2 chain (COL1A2), collagen type VI alpha 1 chain (COL6A1), collagen type VI alpha 2 chain (COL6A2), and collagen type VI alpha 3 chain (COL6A3) were identified as key genes [41]. In Huangshan Black chickens (an indigenous Chinese breed), it was reported that genes, including FABP4, G0/G1 switch 2 (G0S2), PLIN1, SCD, fatty acid binding protein 1 (FABP1), solute carrier family 1 member 6 (SLC1A6), solute carrier family 45 member 3 (SLC45A3), acyl-CoA synthetase bubblegum family member 1 (ACSBG1), lymphocyte antigen 86 (LY86), ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 5 (ST8SIA5), snail family transcriptional repressor 2 (SNAI2), 15-hydroxyprostaglandin dehydrogenase (HPGD), endothelin 2 (EDN2), and thyroid-hormone responsive protein (THRSP), were‌ differentially expressed in thigh muscles with extremely different IMF contents. These genes were found to be significantly enriched in lipid, steroid, and fatty acid biosynthetic and metabolic pathways [42]. Further experiments confirmed that G0S2 can promote the differentiation of intramuscular preadipocytes and IMF deposition by regulating SCD and its downstream gene, patatin-like phospholipase domain containing 2 (PNPLA2) [43]. In Wuliang Mountain Black-bone chickens, association analysis between the polymorphisms of the CCAAT enhancer binding protein alpha (C/EBPα) gene and meat quality traits revealed that a SNP, g.552G > A, is positively correlated with IMF levels in the breast muscle. Such findings suggested that this SNP could potentially serve as a valuable molecular marker for the marker-assisted selection in chickens [44]. In Gushi-Anka F2 chickens, the lipid metabolism-related gene stanniocalcin 2 (STC2) was found to be highly expressed in breast muscle with high IMF content. It was suggested that SCT2 may improve meat quality by altering the ratios of long-chain unsaturated fatty acids (LC-PUFAs) and glycerophospholipids [45]. These studies have identified key pathways and genes regulating IMF content, thereby enriching the genetic basis for individual variations across different chicken breeds.

The IMF content in leg muscles has been suggested to be significantly greater than that in breast muscles. These muscles constitute the majority of chicken meat products [29]. A comparative analysis of differentially expressed genes (DEGs) between the breast and leg muscles of Beijing-you chickens revealed that IMF deposition could be influenced by cell junction-related signaling pathways, such as focal adhesion and ECM‒receptor interactions (Table 1). PPARG and its downstream genes, including LPL, FABP4, THRSP, FABP3, and carnitine palmitoyltransferase II (CPT2), were identified as playing a crucial role in these process [46]. In Wenchang chickens, a comparative gene expression analysis between breast muscle and abdominal adipose tissue revealed that pyruvate and citric acid metabolism play important roles in IMF deposition. These processes were identified as being closely associated with the expression of genes such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH), lactate dehydrogenase A (LDHA), glutathione peroxidase 1 (GPX1), and 1,4-alpha-glucan branching enzyme 1 (GBE1). In contrast, abdominal fat (AF) deposition was reported to depend on fatty acid synthesis and lipid droplet formation, which are regulated by genes such as fatty acid binding protein 1 (FABP1), ELOVL fatty acid elongase 6 (ELOVL6), SCD, and ADIPOQ [47]. Another integrated analysis comparing breast muscle and abdominal adipose tissue of Lushi chickens revealed significant differences in the lipid compositions between IMF and AF. It was identified that the upregulated metabolites in IMF were mainly glycerophospholipids, such as phosphatidylcholines, phosphatidylethanolamines, phosphatidylglycerols, and phosphatidylinositol, while those in AF were primarily glycerolipids, including triacylglycerols and diacylglycerols. Subsequent in vivo and in vitro experiments confirmed that the transmembrane protein 164 (TMEM164) gene might be mainly involved in the positive regulation of IMF deposition and have a certain negative regulatory effect on AF deposition. Meanwhile, the zinc finger protein 488 (ZNF488) gene was found to have a potential unique positive regulatory function on AF deposition [48]. These studies have elucidated the histological variations and molecular mechanisms underlying fat deposition in chickens.

Several studies have reported significant differences in IMF levels in chickens at various developmental stages [49–54]. These differences provide an ideal model for investigating the molecular mechanisms underlying IMF deposition. In Beijing-you chickens, a proteome analysis conducted at 1, 56, 98, and 140 d identified apolipoprotein A1 (APOA1) and heat shock protein family B (small) member 1 (HSPB1) as potential biomarkers for IMF deposition in breast muscle (Table 1) [49]. Integrated proteomic and metabolomic analysis revealed that protein processing and PPAR signaling pathways are involved in promoting IMF deposition. This finding was observed when comparing Beijing-you chickens and Cobb broilers at embryonic day (ED) 12, ED 17, and 1 d and 14 d post-hatch [50]. A transcriptome analysis conducted from 3 to 18 weeks in Beijing-you chickens discovered that genes related to energy metabolism, including acyl-CoA thioesterase 9 (ACOT9), cholesteryl ester transfer protein (CETP), lipin 1 (LPIN1), diacylglycerol o-acyltransferase 2 (DGAT2), retinol binding protein 7 (RBP7), fructose-bisphosphatase 1 (FBP1), and phosphorylase kinase regulatory subunit alpha 1 (PHKA1), are likely to play a role in regulating IMF deposition in breast muscle [51]. In thigh muscles of Beijing-you chickens, a proteomic analysis conducted at 150, 300, and 450 d revealed that the IMF transport and deposition process is accompanied by the processes of PPAR, MAPK, focal adhesion, and ECM–receptor interactions signaling pathways. Proteins such as apolipoprotein C3 (APOC3), APOA1, stathmin 1 (STMN1), HSPB1, p21 (RAC1) activated kinase 2 (PAK2), TGF-β, apoptosis-inducing enzyme caspase-3 (CASP3), COL1A2, collagen type IV alpha 1 chain (COL4A1), laminin subunit beta 4 (LAMB4), and THBS1 were found to be significantly enriched in these pathways [52]. In Jingxing-yellow chickens, a transcriptome analysis from ED 12 to 180 d identified several core genes associated with high IMF content in the breast muscle. These genes include ENSGALG00000041996, L3MBTL histone methyl-lysine binding protein 1 (L3MBTL1), TNFAIP3 interacting protein 1 (TNIP1), histone acetyltransferase 1 (HAT1), and BEN domain containing 6 (BEND6). Among these genes, L3MBTL1, TNIP1, HAT1, and BEND6 have also been shown to be correlated with low AF content [53]. Another recent transcriptome analysis conducted at 7, 35, 63, 91, and 119 d in Jingxing-yellow chickens identified that signaling pathways, including adipocytokine, MAPK, mTOR, FoxO (forkhead box, sub-group O) and TGF-β, are associated with TG and phospholipids contents in breast muscles. Ribosomal protein S6 kinase B1 (RPS6KB1), BRCA1 DNA repair associated (BRCA1), cyclin dependent kinase 1 (CDK1), ribosomal protein S3 (RPS3), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PPARGC1A/PGC-1α), acyl-CoA synthetase long chain family member 1 (ACSL1), NADH:ubiquinone oxidoreductase subunit AB1 (NDUFAB1), NADH:ubiquinone oxidoreductase subunit A9 (NDUFA9), ATP synthase beta chain, mitochondrial (ATP5B), and protein kinase AMP-activated non-catalytic subunit gamma 2 (PRKAG2) were suggested to be candidate genes that may affect IMF deposition [55]. These studies have shown that, in general, chickens exhibit higher IMF deposition during the finisher phase compared to the rapid muscle development period (grower phase). Post-hatching, the differences in the rate of IMF deposition among different chicken breeds can be attributed to their distinct growth and developmental patterns. These findings have identified candidate genes for the enhancement and targeted regulation of chicken IMF. The developmental patterns and underlying mechanisms of IMF still require further investigation.

Environmental factors and gender have been suggested as potential factors that may influence IMF deposition in chickens. Several studies have reported on the impact of environmental factors and gender on IMF. In Beijing-you chickens and Lueyang black-boned chickens (Chinese indigenous breeds), caged systems have been found to be more conducive to IMF deposition than free-range systems [56, 57]. Further analysis revealed that the DEGs, particularly those genes within the PPAR signaling pathway with upregulated expression, such as angiopoietin-like 4 (ANGPTL4), CD36, FATP1, fatty acid transport protein 4 (FATP4), and perilipin 2 (PLIN2) in the leg muscles of caged versus free-range Lueyang black-boned chickens, are associated with IMF deposition (Table 1) [56]. Exercise volume may be one of the main reasons for the differences in IMF deposition in chickens caused by different housing systems. A recent study confirmed that free-range chickens with high levels of physical activity have lower IMF deposition than caged chickens with limited movement space [58]. In Beijing-you chickens, the interaction between gender and housing systems was found to have no impact on IMF deposition [57].

The conclusions regarding the impact of gender on IMF deposition in chickens are inconsistent. Studies in Cobb 500, Ross 308, Beijing-you chickens, Xueshan chickens, and Daheng broilers have shown that females have higher IMF contents than males [57, 59–61]. In female Daheng broilers, the upregulated expression of the PLIN2 gene was identified as being positively correlated with IMF contents in breast muscles. Subsequent cellular experiments confirmed that PLIN2 enhanced IMF deposition by promoting the proliferation and differentiation of intramuscular preadipocytes while inhibiting apoptosis [59]. These studies emphasized the critical roles of the PPAR signaling pathway and the PLIN2 gene in IMF formation. Several other studies reported that gender has no impact on IMF content in chickens (e.g., White-tailed yellow native chickens and Pearl gray guinea fowl) or that it was higher in males (Ross 308) [54, 62, 63]. This may be partly due to breed-specific characteristics or the long-term reshaping of lipid metabolism pathways through natural or artificial selection. Research has shown that the interactions between breeds and gender significantly influenced the IMF levels in chickens [60]. Moreover, the impacts of the interactions between gender and environment factors on IMF deposition cannot be overlooked, even though one of the aforementioned studies showed no significant effects of this interaction on IMF in Beijing-you chickens [57]. This is a complex mechanism that requires more sophisticated models to accurately evaluate the multifaceted interactions between genetic, environmental, and physiological factors. For example, evaluating the impact of housing systems on chicken IMF content is complicated by the challenge of accounting for random errors from the consumption of exogenous substances, such as insects and grains, under free-range conditions. Developing an optimal free-range model is urgently needed to advance research on the effects of environmental factors and rearing practices on IMF deposition.

With the advancement of high-throughput sequencing technology and the efforts of researchers, new breakthroughs have been made in understanding the underlying regulatory mechanism of IMF deposition in chicken at the cellular level. The first study to apply single-cell RNA sequencing (scRNA-seq) to investigate the heterogeneity of breast muscle cells in Jingxing-yellow chickens identified that genes APOA1, COL1A1, and ADIPOQ can serve as biomarkers for intramuscular fat cells in chickens (Table 1) [64]. A subsequent latest large-scale genetic analysis of an IMF-selected chicken population, which combined whole-genome resequencing, scRNA-seq, and transcriptome analysis, demonstrated that DNL predominantly occurs in myocytes, with only minor contributions from adipocytes, and is key to the formation of IMF in chicken muscle tissue. Fatty acid synthase (FASN) was identified as the crucial enzyme driving this process [65]. This finding reshaped the prevailing theory that DNL in poultry mainly occurs in the liver, with little to none occurring in muscle and adipose tissue [66, 67]. A causal mutation, rs315349829, located upstream of the FASN gene was identified. It was found to positively correlate with the key IMF components, C14:0 and C16:0 fatty acids, by upregulating FASN expression in chicken breast muscle tissue [65]. At cellular levels, the functions of two genes, tissue inhibitor of metalloproteinases 2 (TIMP2) and insulin-like growth factor binding protein 7 (IGFBP7), have been demonstrated. A co-culture model of chicken satellite cells and intramuscular adipocytes showed that TIMP2 could promote IMF deposition through the ECM–receptor interaction signaling pathway [68]. IGFBP7 was shown to promote the proliferation and differentiation of primary myoblasts and intramuscular preadipocytes in chicken. This was suggested to be achieved by the binding of transcriptional activators myoblast determination factor (MyoD), myogenin (MyoG), and C/EBPα to the IGFBP7 promoter region [69]. These findings have enriched our insights into fat metabolism in poultry muscle tissue.

Although existing studies have elucidated the genetic basis of IMF deposition in chickens from the perspectives of interspecific and intraspecific differences, several limitations remain:Current genetic mechanism studies have predominantly focused on specific genes or pathways (e.g., FABP4 and PPARγ), yet they lack systematic integration of multidimensional regulatory networks (e.g., the interactions among SNPs, epigenetic modifications, and noncoding RNAs (ncRNAs)).The explanatory power of existing molecular markers (e.g., the BB genotype of FABP4) for the IMF phenotype remains unevaluated, and their validation across breeds is insufficient (for example, the stability of FABP4 expression among indigenous breeds is unclear).Muscle tissue-specific mechanisms have yet to be fully elucidated, particularly whether the IMF differences between breast muscle and leg muscle stem from distinct adipogenic precursor cell differentiation trajectories or specific metabolic pathways.Research on gene–environment interactions is limited, as the synergistic effects of nutritional interventions and genetic backgrounds (e.g., PPARG polymorphisms) remain unquantified.

Future research directions include: Utilizing scRNA-seq, and multiomics technologies to elucidate the spatiotemporal dynamics of IMF deposition (e.g., the programming of MSCs during embryonic development and the temporal sequence of muscle differentiation in the growth phase). Developing comparative models of muscle heterogeneity (e.g., organoids) to identify regulatory nodes of IMF heterogeneity in chickens. Constructing a polygenic integration scoring model (integrating SNPs, epigenetic modifications, and ncRNA targets) and combining it with artificial intelligence models to optimize breeding strategies for “high IMF–fast growth” synergies. Exploring tissue-specific gene-editing technologies (e.g., targeted clustered regularly interspaced short palindromic repeats (CRISPR) delivery systems) to provide new paradigms for the precise regulation of IMF.

By integrating multiomics technologies, elucidating the dynamic regulatory network of IMF, and analyzing its interactions with the environment, future research will further uncover the complex regulatory mechanisms of IMF and provide a solid theoretical foundation and technical support for breeding high-quality chicken meat.

Epigenetic modifications of genetic material are known to include DNA cytosine methylation and N⁶-methyladenosine (m⁶A) modification of RNA. These modifications have been proven to regulate IMF deposition in chickens (Table 1). A genome-wide methylation analysis revealed that high IMF levels were highly correlated with the hypermethylation of the promoters of three genes: ATP binding cassette subfamily A member 1 (ABCA1), COL6A1, and glutathione S-transferase theta 1-like (GSTT1L). The expression levels of these genes were significantly negatively correlated with their methylation levels. ABCA1 has been demonstrated to play a major role in cholesterol efflux, maintaining cholesterol homeostasis and lipid metabolism in adipocytes. Its hypermethylation and down-regulated expression may contribute to higher IMF content. COL6A1 encodes a component of collagen, a major structural protein in muscle tissue. The hypermethylation and subsequent downregulation of COL6A1 could affect muscle fiber properties, leading to changes in meat tenderness and texture. GSTT1L has been identified as a participant in glutathione metabolism, which is related to antioxidant defense and cellular aging. The hypermethylation and downregulation of GSTT1L may affect meat quality by influencing oxidative stability and aging processes in muscle tissue [70]. Another integrative multiomics analysis in Jingxing-yellow chickens identified phospholipase A2 group IVF (PLA2G4F) as a differentially methylated gene (DMG) that could be a key candidate influencing IMF deposition during chicken development. This DMG was significantly enriched in the glycerophospholipid metabolism pathway. Its downregulation has been shown to suppress the degradation of unsaturated fatty acids through multiple mechanisms, including inhibiting the activity of key enzymes involved in fatty acid catabolism (e.g., acetyl-CoA dehydrogenase, lipoxygenase, and fatty acid dioxygenase) and activating the PPARγ signaling pathway and its downstream target genes [71]. These findings reveal potential genes and pathways related to muscle development and meat quality through DNA methylation. These genes may serve as epigenetic markers and regulatory targets for evaluating meat quality in chickens.

Beyond transcriptional silencing via DNA methylation, post-transcriptional RNA modifications are emerging as an equally pivotal layer of epigenetic regulation. In Jingyuan chickens, studies on breast muscle tissues at different developmental stages have revealed that the m⁶A-induced ferroptosis pathway is a novel target for regulating IMF deposition. Leiomodin 2 (LMOD2) and several other m⁶A-regulated DMGs have been demonstrated to be potential regulatory factors [72]. Weighted gene co-expression network analysis and in vitro cell modeling further identified m⁶A methylation-mediated cubilin (CUBN), multiple EGF-like domain 10 (MEGF10), block of proliferation 1 (BOP1), and bone morphogenetic protein receptor 2 (BMPR2) could serve as potential candidate genes for regulating muscle development and IMF deposition [73]. A cross-tissue comparative analysis of m⁶A modifications between the breast and leg muscles revealed that enoyl-CoA hydratase 1 (ECH1), branched chain amino acid transaminase 1 (BCAT1), and cytochrome P450 family 1 subfamily B member 1 (CYP1B1) are key DMGs involved in the regulation of muscle lipid metabolism [74]. These studies reveal the epigenetic basis of chicken IMF regulation and establish a framework for optimizing chicken meat quality through precision breeding.

With advancements in epigenetics, recent studies have confirmed that endogenous noncoding RNAs (ncRNAs), including microRNAs (miRNAs), long noncoding RNAs (lncRNAs), and circular RNAs (circRNAs), play multiple regulatory roles in the formation and deposition of IMF in chickens [75, 76].

The metabolizable energy (ME) content of the diet has been shown to significantly influence the body composition of chickens [6]. An increase in the dietary ME level was shown to be correlated with improvements in IMF deposition and meat quality. For instance, in Huxu yellow-feathered chickens, an indigenous Chinese breed, the diameter and cross-sectional area of breast myofibers were observed to decrease linearly, and the myofiber density was increased with increasing ME intake during the finisher phase. These changes enhanced the IMF content and tenderness of the chicken meat. The optimal quality and flavor of chicken meat were achieved when the dietary ME level reached 3,180 kcal/kg. This increase is likely linked to the consumption of a high-energy diet, which appears to promote the mRNA expression of the FABP3 and APOB genes, thereby facilitating the increased IMF deposition in muscle tissues [112]. However, diets with increased ME might also decrease feed utilization efficiency, as an increased AF rate has been exhibited [113]. This contradiction can be explained by the dual effects of high-energy diets. While such diets have been shown to promote IMF deposition, they also led to excessive fat accumulation in non-target areas, such as the abdomen. Excessive AF is known to be associated with a reduction in the economic value of the carcass, as it does not contribute to commercial value. High-energy diets were also suggested to increase the metabolic burden on chickens, potentially altering energy allocation. This shift may result in more energy being used for fat synthesis and storage rather than for growth and production, which could contribute to a decrease in feed conversion efficiency [114]. These findings suggest that relying solely on high-ME diets to improve meat quality may not be the most effective strategy. Future research should optimize feed formulations to enhance meat quality while minimizing the adverse effects on feed utilization efficiency.

Research findings on the impact of low-ME diets on chicken IMF deposition and meat quality are inconsistent. For example, in Ross 308 broilers, diets with ME levels 23.9 kcal/kg and 59.75 kcal/kg below the control diet were found to significantly increase the IMF content, pH_15min, meat color L^* values and antioxidant capacity, but also to negatively affect the WHC of the breast muscle [115]. A reduction in dietary ME by 100 kcal/kg relative to the control group was reported to not influence meat quality parameters, including WHC, pH, meat color L^* values, and tenderness [116, 117]. Up to now, research on the effects of low-energy diets on IMF deposition and meat quality in chickens remains limited. Future research should investigate the interaction between dietary energy levels and various factors such as genetic background, age, and breed, and assess how these interactions might influence IMF deposition and meat quality.

Recent research has confirmed that the ratio of dietary energy to protein can significantly affect muscle protein and fat levels (Table 2). For example, in Beijing-you chickens, a diet containing 11.51 MJ/kg of ME and 15% CP was shown to maximize the improvement of IMF levels and flavor in the breast meat [6]. In Taihe silky fowl (an indigenous Chinese breed), a diet with 12.56 MJ/kg of ME and 15% CP was found to optimize the content of IMF, tenderness, flavor, and feed conversion ratio (FCR) [122]. These varying results are likely attributed to interactions between energy and protein intake, as well as the supplementation of essential amino acids and the balance among amino acids. Amino acids are fundamental not only for muscle protein synthesis but also as essential regulatory factors in metabolic pathways, antioxidant systems, and enzymatic processes [8, 9]. Optimizing the dietary amino acid profile is crucial for mitigating the negative effects of low-protein diets. Studies have shown that the impairment of production performance, muscle composition, and meat quality characteristics in broiler chickens could be prevented by achieving amino acid balance, for instance by adjusting the ratio of digestible threonine (dThr) to digestible lysine (dLys) and the ratio of digestible arginine (dArg) to dLys, even when the dietary CP content was reduced to 17% or lower. In fact, such adjustments have been found to improve meat quality [123, 124]. To ensure meat quality under low-protein diets, it is deemed essential not only to balance the dietary energy-to-protein ratio but also to meet the requirements of essential amino acids, such as methionine (Met), Thr, and Arg, as well as nonessential amino acids, such as glycine (Gly) [123].

Met is considered the first limiting amino acid in corn-soybean meal diets for chickens and has been suggested to significantly impact the meat quality of broilers (Table 2). Studies have found that increasing the dietary Met content to 0.65% during the starter phase and to 0.57% during the finisher phase significantly increased the pH, decreased the meat color L^* value, and reduced the cooking loss of breast muscle [8]. This effect appeared to be almost dose dependent and was not influenced by the source of Met, whether it was DL-Met or a Met dipeptide [125]. When dietary Met was supplemented, reductions in IMF deposition and the a^* value of meat color were observed, along with enhancements in the antioxidant capacity of breast muscle and alleviation of lipid peroxidation caused by heat stress [8, 126]. Met supplementation has been demonstrated to have positive effects on chicken meat quality to some extent, although it might reduce IMF deposition. It has been proposed that Met might reduce the activity of pyruvate kinase, which could inhibit glycolysis and lactate accumulation. Such an action might increase the pH of the breast muscle. The L^* value and cooking loss of the meat were found to be decreased [127–129]. The increased antioxidant capacity of the breast muscle may be attributed to its contribution to the biosynthesis of the endogenous antioxidant glutathione [8, 130].

Lys is recognized as the second limiting amino acid after Met in the basal diet for chickens [131]. As displayed in Table 2, supplementing diets with Lys alone has been shown to significantly improve broiler production performance, such as increasing carcass weight, breast muscle weight, and leg muscle weight, without altering meat quality indicators such as meat color, pH, and the IMF content [132]. The interactions between Lys and other amino acids have been observed to have significant impacts on meat quality. A linear reduction in body fat deposition was observed in Ross 308 broilers when diets exceeded the National Research Council (NRC 1994) recommendations for Lys and Met. Particularly, when Lys and Met levels were increased by 40% above the recommendations, fat in the breast and leg muscles was reduced by 35% and 27%, respectively, along with a corresponding decrease in AF [133]. Meat quality characteristics have also been observed to be influenced by the degree of amino acid balance in the diet. For instance, when the levels of other essential amino acids in the diet were reduced (AAs −), meat with a relatively high pH (pH > 6.0), darker color, and greater WHC could be resulted from a lower Lys level. Conversely, meat with a lower pH (pH < 5.85), lighter color, and poorer WHC could be resulted from a combination of a lower Lys level and increased levels of other essential amino acids (AAs +) [134]. Under a low-protein diet, the carcass yield and percentages of crude protein, total fat, and moisture in the breast muscle of broilers have been shown to be maintained with adequate supplementation of Lys and Met, even when the dietary crude protein level was 15% [135]. These findings underscore the regulatory effects of the interaction between Lys and other amino acids on meat quality traits, as well as the importance of amino acid balance in broiler nutrition and management.

Appropriate Arg supplementation has been shown to have positive effects on muscle development and IMF deposition in broiler chickens (Table 2). A dietary Arg level of 100.39% of the recommended amount in the Ross 308 Nutrition Specifications was indicated to maximize muscle yield without affecting AF deposition [136]. Lipid metabolism patterns in broilers were detected to be altered when the intake of Arg exceeded the recommended levels. For instance, increasing the dietary dArg concentration to 168% of the recommended level was shown to not only increase the weight and IMF content of the breast muscle but also reduce AF deposition and plasma levels of cholesterol and TG in broilers. These results could be attributed to the fact that Arg supplementation upregulated the expression of genes associated with fat synthesis in muscles, such as FASN and LPL, whereas these genes were down-regulated in AF. This dual action modulated the distribution of fat across body tissues [137, 138].

Feeding Arbor Acres broilers a diet with a high tryptophan (Trp) level (Trp, 0.27%) during the last 3 weeks before marketing has been reported to tend to reduce the drip loss of breast meat. It was suggested that a high level of Trp might enhance the juiciness of chicken meat (Table 2) [139]. This promoting effect could be attribute to Trp's ability to maintain the functional integrity of muscle cell membranes and activate antioxidant enzymes such as glutathione peroxidase and catalase. These actions reduced the loss of intracellular water and inhibit lipid peroxidation and muscle cell membrane damage, thereby potentially improving meat quality [139–142].

BCAAs, including leucine (Leu), isoleucine (Ile), and valine (Val), are acknowledged as constituting an important class of essential amino acids in muscle tissue [143–145]. The transamination of BCAAs primarily occurs in skeletal muscle. Research has indicated that the mTOR signaling pathway in the skeletal muscles of neonatal chicks could be activated by a high Leu diet [146], and this activation promoted protein synthesis while inhibiting its degradation [147]. Similar findings have also been consistently confirmed in both animal and human studies [13]. The regulation of chicken meat quality has been shown to be influenced by Leu and its derivatives (Table 2). In Ross 308 broilers, it was shown that the adverse effects of low-protein diets on growth, development, and meat quality, including muscle yield, WHC, pH, and meat color (a^*, b^*, and L^*), were reversed when the diets were supplemented with Leu or its metabolite β-hydroxy-β-methylbutyrate [148]. Adjusting the ratio of BCAAs in the diet, especially increasing the dietary levels of Ile and Val to 150% of the required amount was suggested to increase the concentration of free glutamine, a primary flavor component, in the breast meat of broilers [149]. Under heat stress conditions, the yield of broiler breast meat was found to decrease when additional dietary BCAAs (1.0, 0.25, and 0.25 g/kg of L-Leu, L-Ile, and L-Val, respectively) were supplemented. This negative impact might be due to the antagonistic effects between Ile and Val [150]. Although antagonistic effects among BCAAs have been noted in broilers, the underlying mechanisms remain to be fully elucidated [151, 152]. Future research is needed to investigate the interactive mechanisms among BCAAs and their impact on meat quality to inform more targeted strategies for enhancing meat quality in broilers.

Omega-6 (ω-6) and omega-3 (ω-3) PUFAs are essential LC-PUFAs. In modern diets, a deficiency of ω-3 PUFAs is leading to an imbalance in the intake ratio of ω-6/ω-3 PUFAs, which is considered to pose a challenge for human health. The need for producing poultry meat rich in ω-3 PUFAs has gained attention among researchers [153]. It has been determined that the content of ω-3 PUFA, including alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) in muscle tissue could be significantly increased, and the ω-6/ω-3 PUFAs ratios could also be reduced, with the dietary supplementation of ω-3 PUFA sources [10]. These desired effects could be achieved by supplementing with 1% fish oil, canola oil, or flaxseed oil [154], 5.5% canola oil [155], or 1%–4% DHA-rich microalgal biomass [156].

A lower dietary ω-6/ω-3 PUFA ratio may be detrimental to the antioxidant capacity of muscle tissue (Table 3). Studies have shown that the antioxidant capacity of muscle on the 7^th d of storage was significantly reduced when the ratio was adjusted to 6:1–2:1 [164]. Further reducing the ratio to 2:1–1:1 has been found to accelerate muscle oxidation within 48 h post-mortem [165]. This phenomenon might be attributed to the oxidation susceptibility of ω-3 PUFAs and their accumulation in muscle tissue. When supplementing with ω-3 PUFAs, it is important to stabilize through combination with antioxidants like vitamin E or soybean isoflavones to improve meat product stabilities [163, 166]. An appropriate supplementation of ω-3 PUFAs seems to be beneficial to the antioxidant performance of chicken meat. For example, diets supplemented with 1 g/kg of microalgae, such as Chlorella vulgaris, Spirulina platensis, or Amphora coffeaeformis, have been discovered to reduce the malondialdehyde (MDA) and protein carbonyl levels in breast muscle and enhance superoxide dismutase (SOD) activity [167].

The source of dietary ω-3 PUFAs has also been detected to significantly impact the growth performance of broilers (Table 3). Studies have shown that the improvements in the production performance of broilers, including their final body weight, FCR, protein efficiency ratio, dressing percentage, and muscle percentage, were achieved when using fish oil or flaxseed oil as a source of ω-3 PUFAs and the dietary ω-6/ω-3 PUFAs ratio was adjusted to 4:1 or 2.5:1 [160]. It was observed that using DHA-rich Aurantiochytrium acetophilum biomass as an ω-3 PUFA source and adjusting the ratio to approximately 3:1 could negatively affect body weight gain (BWG), FCR, and breast muscle weight, and downregulate the expression of key signaling molecules in muscle protein synthesis, including the mRNA levels of mTOR and ribosomal protein S6 (S6), as well as the protein ratios of p-S6/S6 and p-S6 Kβ1/S6 Kβ1 [168]. A fishy odor in chicken meat was supposed to be induced when fish-derived products were used as PUFA sources, which might reduce market acceptance [165, 169, 170]. When selecting ω-3 PUFA supplements, it is necessary to consider the impact of their source on the growth performance and product acceptability.

In practice, the source, type, and dosage of ω-3 PUFAs, as well as their interactions with other nutrients in the diet should be taken into account to optimize broiler growth performance and product characteristics. Adjusting dietary ω-6/ω-3 PUFA ratios or combining them with specific amino acids has been suggested to further improve IMF and meat quality [158, 159]. The authors conclude that a dietary ω-6/ω-3 PUFA ratios between 4:1 and 2.5:1 is ideal, but attention should be given to the source of ω-3 PUFAs and the supplementation of antioxidants. Considering the promoting effects of LC-PUFAs on the proliferation of muscle stem cells (MuSCs) [171] and the differentiation of FAPs [172], future research should explore the regulatory mechanisms of LC-PUFAs on muscle development and adipogenesis in chickens at the cellular level.

Conjugated linoleic acids (CLAs) are positional isomers of linoleic acid [173], and have been confirmed to perform multiple biological functions, such as regulating lipid metabolism and preventing cancer, atherosclerosis, diabetes, and obesity in the body [174–178]. In chickens, diets supplemented with 1.5%–2% CLAs have been found to significantly alter the fatty acid composition in muscle tissue. It was detected that these diets increased the content of CLAs and saturated fatty acids [179–182] and the ratio of ω-6/ω-3 [183], along with a decrease in the levels of monounsaturated and polyunsaturated fatty acids [182, 184]. The effects of CLAs on chicken IMF content have been observed to dose-dependent. Low concentrations (0.25%–1%) of CLAs were observed to promote IMF deposition [185, 186], whereas high concentrations (1.8%–2%) were found to have the opposite effects [179, 185]. An appropriate supplementation of CLAs has been shown to have positive effects on the improvement of chicken meat quality. It was shown that diets supplemented with 0.25%–2% CLAs reduced the shear force and b^* value of breast muscle [185, 186], and that 1.5% CLAs enhanced the antioxidant capacity of chicken meat [181]. Potential interactions have been detected between CLAs and dietary lipids. Compared to supplementation with 4.2% CLAs alone, a diet supplemented with 2.1% CLAs and 3.5% soybean oil was found to be more effective in promoting the deposition of CLAs in chicken muscle in a previous study [187]. Further research has also confirmed that the increased deposition of CLAs in muscle was not merely the result of lipid accumulation [188]. It has been shown that the reduction in the content of polyunsaturated fatty acids and the increased ω-6/ω-3 ratio induced by CLAs in muscle could be alleviated by incorporating CLAs and ω-3 fatty acids into the diet [189, 190]. During the starter phase, the BWG of broilers was shown to be negatively affected by dietary supplementation with 1% CLAs, and increasing the dietary energy level was observed to be ineffective in compensating for this impact [191]. An accurate level of CLAs is considered essential for optimal broiler production. Future studies should optimize CLAs supplementation and investigate its interactions with other nutrients to enhance fatty acid utilization and to improve the balance of fatty acids in chicken meat.

Maternal nutrient intake and energy metabolism have been recognized as having direct impacts on offspring growth performance and meat quality (Table 5). It has been demonstrated that the offsprings from breeders with high residual maintenance requirement (RME_m) exhibit greater breast yield (29.5%) and tenderness (4.7% lower force/g) compared to those from breeders with low RME_m. Offsprings’ growth and development performance have also been observed to be inversely correlated with the residual feed intake (RFI) of their mothers. The optimal body weight gains at market age were observed in the offsprings from mothers with low RFI and high RME_m [216]. Specific maternal diets, such as 17.5% CP with 11.51 or 11.92 MJ/kg ME, have been discovered to enhance the growth performance of offsprings during the starter phase, while 15.5% CP with 11.51 MJ/kg ME has been noted to enhance dressing percentage and meat color during the finisher phase [217]. In Arbor Acres broilers, it has been found that moderate maternal energy restriction (−2.34 MJ/kg and −3.51 MJ/kg) could enhance the muscular antioxidant capacity of the offsprings, but excessive restriction (−5.85 MJ/kg) might be harmful [218]. Maternal energy restriction has been reported to increase the IMF content in offspring breast muscle at 28 d of age [218, 219]. These effects did not persist into the finisher stage, which suggests that the maternal effects are more significant during the early growth stage. It was also reported that maternal energy restriction improved the WHC of muscle at market age in Arbor Acres broilers [218].

Maternal energy restriction has been found to influence the phenotypic characteristics of myofibers of offsprings (Table 5). In Arbor Acres broilers, an increase in maternal energy restriction has been detected to be associated with a decrease in the diameter of breast myofibers in the offsprings, while their density has increased [220]. Similar findings have also been observed in fat-line broilers [219]. The results in lean-line broilers have been shown to be opposite, which could imply an interaction between maternal energy intake and broiler strains [219]. Broiler breeders of different strains have been found to have varying energy requirements for their own maintenance and the embryonic development of their offsprings. The different results observed in fat-line broilers could be attributed to the fact that undernutrition leads to insufficient myofiber development [221, 222]. Future research should aim to clarify the regulatory mechanisms underlying this interaction and its impact on the meat quality of offsprings.

The growth performance and meat quality of offsprings have been discovered to be regulated by maternal Met intake (Table 5). It has been shown that a maternal diet supplemented with 1% coated-Met increased the final body weight, dressing percentage, and muscle weight of the offsprings, as well as improved the pH_45min and tenderness of the breast muscle, along with decreasing the meat color a^* value. Excessive Met supplementation, such as 2%, has been shown to be harmful to the growth performance of the offsprings [223]. Supplementation of the paternal diet with 1% coated-Met has also been shown to have effects similar to those of the maternal diet, which increased the WHC and meat color L^* and a^* values in the offspring’s muscles [224]. These results emphasize the importance of parental amino acid nutrition for muscle development and meat quality in offsprings.

The supplementation of maternal trace elements has been shown to promote muscle development in offsprings (Table 5). An increase in the breast muscle percentage of offspring chicks during the finisher phase has been reported when the maternal diet was supplemented with 100 mg/kg zinc sources, such as zinc sulfate (ZnSO₄) or methionine hydroxy analog-chelated zinc [225]. Their myofiber width was detected to be significantly increased when maternal diets were supplemented with 50 mg/kg or 300 mg/kg of ZnSO₄ [226]. The enhancement of muscle development in the offsprings has been proposed to be attributed to the detected deposition of zinc in hatching eggs, which promoted protein synthesis by activating the AKT/mTOR signaling pathway and reduced protein degradation by inhibiting the ubiquitin‒proteasome system pathway [225, 226]. A recent study has indicated that the deposition of Fe, Mn, and Zn in the yolks of hatching eggs was increased to some extent by supplementing the maternal diet with 500 mg/kg of collagen peptide chelated trace elements, providing 11.65 mg/kg Fe, 8.1 mg/kg Mn, and 32.88 mg/kg Zn. An increase in the breast muscle rate of the offsprings was observed due to this supplementation, which promoted protein metabolism and upregulated the expression of myogenic factors by activating the IGF-1 signaling pathway [227]. These findings provide a theoretical basis for improving muscle development in offsprings through maternal trace element supplementation.

The meat quality of offsprings has also been shown to be influenced by the sources of trace elements in maternal intake (Table 5). It was shown that the WHC and antioxidant capacity of the breast muscle of offsprings were significantly enhanced by supplementing the diets of Lingnan-yellow chickens (an indigenous Chinese breed) and Ross 308 broiler breeders with 0.3 mg/kg of organic selenium, in the form of selenomethionine, selenium-enriched yeast, or hydroxy-selenomethionine [228, 229]. This significant effect was not observed in Ross-308 broilers during the finisher phase [228], suggesting that there might be an interaction between the supplementation of maternal trace elements and chicken breeds. The interaction may be attributed to variations in the genetic structure among different chicken breeds. Chinese local chicken breeds, which are widely recognized as typically having a greater proportion of oxidative myofibers and better meat quality [230], might be more sensitive to trace element metabolism. This characteristic could lead to the carry-over of maternal effects into the finisher phase. Future research needs to delve into this interaction and explore the underlying mechanisms affecting the persistence of maternal effects.

Maternal diets supplemented with 80 mg/kg zinc, in the form of either ZnSO₄ or zinc glycine (Zn-Gly), have been discovered to enhance antioxidant capacity and alleviate oxidative stress in the offsprings, thereby reducing embryo mortality under heat stress (Table 5). The observed improvement has been confirmed to be attributed to the activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway and the reduction in CASP3 activity, both of which have been identified to slow down oxidative stress injury and tissue cell apoptosis [231]. Organic zinc in maternal diets was found to exert more pronounced effects on offsprings than inorganic zinc [231, 232], and it was found to improve the b^* value of meat color [232]. Maternal supplementation with a combination of organic trace elements, including Fe, Cu, Mn, and Zn, was observed to increase body weight and FCR in the offsprings during the starter phase [233]. Further research is needed to understand the impact of trace element supplementation in maternal diets on IMF deposition in the offsprings.

Regarding vitamins, it has been demonstrated that maternal diets supplemented with vitamin A have a relatively limited impact when compared to feeding the offspring directly (Table 5). It was reported that a maternal diet supplemented with 21,600 IU/kg of vitamin A only improved the pH_24h in the breast muscle of offsprings at market age. However, feeding offsprings a 5,000 IU/kg vitamin A diet directly was found to not only significantly improve the pH_45min and tenderness of the breast muscle but also enhanced the WHC and meat color, specifically the L^* and b^* values [234]. These findings suggest that the effects of vitamin A supplementation in maternal diets on the offsprings’ meat quality might be limited.

Some studies have shown that the interaction between maternal dietary vitamin E levels and oil sources significantly affected offsprings’ meat quality (Table 5). When soybean oil was the source, maternal vitamin E supplementation linearly reduced the breast muscle color; when fish oil was used, the same vitamin E treatment linearly increased the pH_24h of the breast muscle, and at a dose of 187 mg/kg, it resulted in the lowest drip loss [235]. These results reveal the oil source-dependent effects of maternal dietary vitamin E on the meat quality of offsprings. Although co-supplementation with 100 mg/kg vitamin E in both maternal and offspring diets reduced the drip loss of breast meat, it also impaired the antioxidant capacity of offsprings [236]. Long-term high-dose vitamin E supplementation may lead to its accumulation, which can produce additive effects and thereby promote the occurrence of peroxidation in the offsprings [237]. These findings emphasize the necessity of balancing vitamin E intake between mother and offsprings. Further research is needed to determine the optimal dosage of vitamin E supplementation for breeders and to elucidate the specific mechanisms by which it interacts with oils to regulate the meat quality of offspring broilers.

Several specific phytochemicals that are supplemented in maternal diets have been proven to promote muscle development and growth performance in offsprings (Table 5). For instance, supplementing maternal diets with genistein (GEN, 40 mg/kg) was shown to increase embryonic length and weight, as well as the width of the proliferative zone in the tibial growth plate of offspring embryos. Its underlying mechanisms were demonstrated to involve the regulation of insulin-like growth factor-binding protein 3 (IGFBP3) gene expression, the activation of glycolipid metabolism pathways, and the enhancement of antioxidant capacity and immune function [238]. Maternal supplementation with GEN was found to improve body weight gain and the rate of breast or leg muscle development in offspring post-hatch, while also optimizing the morphology of the intestinal villi and the structure of the gut microbiota, thereby alleviating mucosal injury [239, 240]. A maternal diet supplemented with hawthorn-leaf flavonoids (60 mg/kg) was found to exert similar effects on intestinal development and microbial community structure and to enhance offsprings’ growth performance via the IGF-1R/AKT/mTOR signaling pathway [241]. Maternal intake of mulberry-leaf flavonoids (MLF, 30 or 60 mg/kg) was observed to increase body weight gain and the breast muscle rate and to enlarge the cross-sectional area of breast myofibers in the offsprings [242]. These benefits have been suggested to be attributed to the upregulation of Myf5 gene expression and the activation of the Bone Morphogenetic Proteins (BMP)/p-SMAD1/5/9 axis, both of which collectively promote muscle development. Maternal intake of soyasaponin (200 mg/kg) was discovered to interact with vertically transmitted Bifidobacterium adolescentis to produce γ‐aminobutyric acid (GABA). GABA was subsequently identified to modulate offspring intestinal development by inhibiting autophagy and apoptosis pathways associated with microtubule-associated protein 1 light chain 3 (LC3) and CASP3, as well as by promoting proliferation and differentiation pathways mediated by proteins, leucine rich repeat containing G protein-coupled receptor 5 (LGR5) and olfactomedin 4 (OLFM4) [243]. These findings confirm that maternal intake of phytochemicals can positively regulate the growth and development of offsprings by modulating growth pathways and improving gut health. They also imply that maternal phytochemical intake might influence the IMF content and meat quality in the offsprings, warranting further investigation.

In chickens, the influence of maternal fatty acid supplementation on offsprings’ meat quality has not yet been fully explored. Those studies focused primarily on the effects of PUFA supplementation on fatty acid composition of eggs, as well as on growth performance, immune response, and central nervous system development of the offsprings [214]. Fatty acids have been acknowledged as crucial nutrients for embryonic development, providing both energy and functional fatty acids such as essential ω-6 and ω-3 PUFAs. Specific long-chain fatty acids, such as oleic acid, palmitic acid, and arachidonic acid, have been demonstrated to promote the proliferation of MuSCs [171], whereas DHA has been identified to promote adipocyte production and lipogenesis by activating the free fatty acid receptor 4 (FFAR4) in FAPs [172]. Considering the development characteristics of myofibers and adipocytes during the embryonic period, maternal fatty acid supplementation could significantly affect the IMF content and meat quality of offsprings. Future research should focus on the regulatory effects and underlying mechanisms of fatty acid types, sources, and dosages in maternal diets on the IMF content and meat quality of offspring.

IOF has been advocated as a compensation strategy for embryonic nutritional deficiencies to ensure muscle development and meat quality in chicks, and has garnered increasing attention from researchers (Table 6). Injecting nutrients such as synbiotics, vitamins, trace elements, amino acids, and hormone analogs into eggs has been reported to improve broiler meat quality through multiple biological mechanisms. It was found that the percentage of type I myofibers in broiler chicks was significantly increased by the IOF of N-carbamylglutamate (NCG, 2 mg/egg) at 17.5 ED, resulting in enhanced the IMF content, antioxidant capacity, WHC, and tenderness of the breast muscle at market age. This improvement has been demonstrated to be associated with NCG enhancing the gene expression of MSTN and PGC-1α, which in turn activates the gene expression of PPARG and regulating myofiber types [244, 245]. When a combination of inulin and Lactococcus lactis subsp. lactis was employed for IOF at 12ED, a significant reduction in the proportion of type I myofibers and increase type II myofibers at 35 d in Ross 308 broilers were observed [246]. These findings indicate that meat quality can be regulated by IOF via its effects on myofiber types.

Vitamins administered through IOF have been found to improve the quality of chicken meat (Table 6). It was reported that an IOF of 36 mg/egg of vitamin C at 17ED significantly improved the tenderness of breast meat at market age [247]. An IOF of a low dose of vitamin C (6 μg/egg) at 18ED was shown to effectively prevent the toughness of breast meat caused by heat stress during incubation [248]. The IOF of vitamin C at 3 mg/egg at 15ED and at 12 mg/egg at 17ED was observed to enhance the antioxidant performance of broilers post-hatch [247, 249]. An IOF of 60.4 IU/egg of vitamin E or 0.65 mg/egg of canthaxanthin at 17.5ED was discovered to exhibit similar antioxidant effects [250, 251]. These results emphasize the beneficial impacts of IOF of vitamin C and vitamin E on the taste and antioxidant capacity of chicken meat.

The IOF of vitamins has been reported to help reduce the occurrence of wooden breast in broilers (Table 6). Studies showed that the incidence of wooden breast in broilers at market age decreased after the IOF of 25-hydroxyvitamin D₃ (25-OHD₃) was applied at 18 ED. This effect might be attributed to the long half-life of 25-OHD₃, which remains in the muscle tissue for a longer period, thereby potentially alleviating muscle inflammation related to the development of wooden breast [252, 253]. Studies have shown that the effects of IOF on chicken meat quality can vary significantly between genders. In female broilers, a significant decrease in drip loss and meat color, specifically the a^* and b^* values, and an improvement in tenderness at market age were observed after an IOF of 100 μg/egg equol was applied at 7 ED [254]. However, similar results have not been observed in males. These distinct results may be attributed to the gender-specific susceptibility and hormonal responsiveness in broiler chickens, which could explain the observed differences in meat quality. Similar evidence has also been found in another study, which demonstrated that testosterone could promote muscle growth and reduce IMF deposition in roosters but not in hens [255]. These findings underscore the importance of considering the interactions between nutrients and gender when IOF strategies are applied. A deeper investigation into the mechanisms underlying these interactions, particularly in the regulation of IMF and meat quality, would be beneficial for the refinement and optimization of these strategies.

Recently, a study found that IOF of synbiotics (Lactobacillus plantarum+Lupin raffinose family oligosaccharides) at 12ED significantly reduced the IMF content and meat color L^*_45min values in the breast muscles of broilers at market age [256]. The IOF of zinc (60 mg/egg) at 18ED was observed to significantly increase the pH of breast meat at market age, which was superior to that of the control group and the experimental groups fed with zinc only after hatching (100 mg/kg or 200 mg/kg; see Table 6) [257]. The IOF of galactooligosaccharides (3.5 mg/egg) or sodium butyrate (0.6 mg/egg) at 12ED was reported to significantly reduce the IMF content in muscles, but improve the WHC of leg muscles in Ross 308 chickens at 42 d [258]. These findings further confirm the regulatory effects of IOF on IMF and meat quality, and indicate that the administration of certain substances via IOF may not be conducive to IMF deposition in chickens. Current research on embryonic nutrition primarily focuses on the phenotypic characteristics of growth performance and meat quality, but has limited exploration of both IMF deposition and the regulatory mechanisms underlying these phenotypes. Future research should aim to deepen the understanding of these regulatory mechanisms.