High-fat diet-induced anorexia in rats: involving orosensory deficits, gastrointestinal dysfunction, intestinal taste receptor downregulation and dopamine signaling dysregulation

Nov 28, 2025European journal of medical research

High-fat diet causes reduced eating in rats linked to taste problems, digestive issues, lower gut taste sensors, and altered dopamine signals

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Abstract

Total food intake was 41.5% lower and final body weight was 21.8% lower in rats on a high-fat diet compared to controls.

High-fat diet consumption led to a significant degeneration of taste buds, with a 49.13% reduction in count.
was impaired, shown by increased gastric residual rate and decreased small intestinal advancement rate.
Molecular analysis revealed significantly decreased mRNA expression levels of taste receptors T1R1, T1R3, and TRPM5 in the proximal jejunum.
Hypothalamic dopamine levels were significantly lower in rats fed a high-fat diet compared to those on a standard diet.
These findings suggest that disruption in the peripheral-central axis may contribute to associated with high-fat diet consumption.

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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.

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High-fat diet-induced anorexia in rats: involving orosensory deficits, gastrointestinal dysfunction, intestinal taste receptor downregulation and dopamine signaling dysregulation

Abstract

Key numbers

Full Text

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