Frontiers in veterinary science · 2026
Dietary energy levels regulate feed intake of broilers through the brain-gut axis.
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Yang Yiwen, Zhou Ling, Liu Hongjing, Huang Zhiyong, Zhang Jiancong, Lv Li
Аннотация
BACKGROUND: Feed intake (FI) in broilers is significantly influenced by dietary energy levels through the brain-gut axis (BGA), profoundly affecting growth performance. The mechanisms underlying dietary energy regulation of FI and intestinal health via BGA remain unclear.
AIM: This study investigated the effects of low- (LED, 2,900 kcal/kg), medium- (MED, 3,200 kcal/kg), and high-energy diets (HED, 3,500 kcal/kg) on BGA function over 21 days.
RESULTS: We found that increasing dietary energy reduced FI but increased body weight gain and improved feed conversion ratio. MED elevated anorexigenic hormones (serum CCK, hypothalamic POMC) and suppressed orexigenic hormones (serum orexin, hypothalamic AgRP and NPY). HED further enhanced anorexigenic signals (serum PYY, intestinal CCK and PYY) and strongly inhibited orexigenic factors. Both MED and HED activated the hypothalamic Rac1/PI3K/SF1 pathway, upregulating phosphorylated proteins and SF1 expression in the ventromedial hypothalamus. Importantly, MED promoted cecal microbiota balance, whereas HED impaired intestinal barrier function (ZO-1) and induced inflammation.
CONCLUSION: These results suggest that dietary energy levels modulate FI through BGA remodeling, integrating appetite hormones, hypothalamic signaling, and gut health, with high-energy diets increasing weight at the expense of intestinal integrity. Future studies could examine long-term effects and explore targeted interventions to maintain growth while protecting intestinal integrity under high-energy feeding.
AIM: This study investigated the effects of low- (LED, 2,900 kcal/kg), medium- (MED, 3,200 kcal/kg), and high-energy diets (HED, 3,500 kcal/kg) on BGA function over 21 days.
RESULTS: We found that increasing dietary energy reduced FI but increased body weight gain and improved feed conversion ratio. MED elevated anorexigenic hormones (serum CCK, hypothalamic POMC) and suppressed orexigenic hormones (serum orexin, hypothalamic AgRP and NPY). HED further enhanced anorexigenic signals (serum PYY, intestinal CCK and PYY) and strongly inhibited orexigenic factors. Both MED and HED activated the hypothalamic Rac1/PI3K/SF1 pathway, upregulating phosphorylated proteins and SF1 expression in the ventromedial hypothalamus. Importantly, MED promoted cecal microbiota balance, whereas HED impaired intestinal barrier function (ZO-1) and induced inflammation.
CONCLUSION: These results suggest that dietary energy levels modulate FI through BGA remodeling, integrating appetite hormones, hypothalamic signaling, and gut health, with high-energy diets increasing weight at the expense of intestinal integrity. Future studies could examine long-term effects and explore targeted interventions to maintain growth while protecting intestinal integrity under high-energy feeding.