High-fat feeding induced -like changes in young rats alongside taste, gut-motility, intestinal receptor, and dopamine abnormalities.
Evidence
Randomized 27-day rat experiment in 20 male Sprague-Dawley rats found 41.5% lower food intake, 21.8% lower final body weight, fewer taste buds, increased GRR, decreased SIAR, lower proximal jejunal T1R1/T1R3/TRPM5 mRNA, and lower hypothalamic dopamine after high-fat diet.
Caveat
The study used a small male rat sample and measured short-term physiological and molecular changes rather than proving the full peripheral-central causal pathway in humans.
Simplified
OBJECTIVES: To explore how a high-fat diet (HFD) led to in rats via peripheral-central axis integrated dysfunction.
METHODS: Twenty male Sprague‒Dawley rats were randomly assigned to the control group (G1, standard chow; n = 10) or the high-fat diet group (G2; n = 10) for 27 days. Body weight and food consumption were recorded at regular intervals. The gastric residual rate (GRR) and small intestinal advancement rate (SIAR) were used to evaluate . The circumvallate papillae (CVP), proximal jejunum and hypothalamus were collected postintervention. Analyses included analyses of CVP histology (H&E staining), taste receptor type 1 member expression (T1R1/T1R2/T1R3) and transient receptor potential melastatin 5 (TRPM5) through immunohistochemistry and quantitative real-time PCR (qPCR) and hypothalamic dopamine (DA) levels by enzyme-linked immunosorbent assay (ELISA).
RESULTS: Total food intake (41.5% lower) and final body weight (21.8% lower) were significantly lower in the HFD group than in the control group. The morphology of CVP was significantly degenerated by HFD feeding, resulting in a 49.13% reduction in the taste bud count. Gastrointestinal dysfunction was evidenced by increased GRR and decreased SIAR. Although taste receptor expression in CVP remained unchanged, the proximaljejunal mRNA expression levels of T1R1, T1R3, and TRPM5 significantly decreased. Notably, the DA concentration in the hypothalamus was also significantly lower in HFD-fed rats than in control rats.
CONCLUSIONS: HFD consumption effectively induced anorexia in young rats, which was accompanied by gastrointestinal dysfunction, a reduction in taste buds, impaired gut-brain axis taste transduction and a suppressed central DA response. These results indicate that peripheral-central axis impairment may be an important pathological phenomenon in HFD-induced anorexia.
Key numbers
41.5%
Decrease in Food Intake
Food intake in high-fat diet group compared to control group.
21.8%
Decrease in Body Weight
Final body weight in high-fat diet group compared to control group.
49.13%
Reduction in Taste Bud Count
Taste bud count in of high-fat diet group.
Full Text
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Gut-Brain Axis