Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit
Butyrate reduces appetite and activates brown adipose tissue via the gut-brain neural circuit
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DOI：
10.1136/gutjnl-2017-314050
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发表时间：
2018-07-01
期刊：
影响因子：
24.5
通讯作者：
Wang, Yanan
中科院分区：
文献类型：
--
作者：
Li, Zhuang;Yi, Chun-Xia;Wang, Yanan
目的丁酸盐对小鼠和人类具有代谢益处，但其潜在机制尚不清楚。我们的目的是调查丁酸盐对食欲和能量消耗的影响，以及在何种程度上这两个组件有助于丁酸盐的有益代谢effects of butyrate.Design A cute effects of butyrate on appetite and its method of action were investigated in the mice after an intragastric gavage or intravenous injection of butyrate.为了研究饱腹感对丁酸盐代谢益处的贡献，小鼠被喂食含有丁酸盐的高脂肪饮食，并且包括额外的成对喂食组。机械参与的肠-脑神经回路进行了调查，在vagotomised mice.Results一个可爱的口服，但不是静脉注射，丁酸管理减少食物摄入量，抑制食欲神经元，表达神经肽Y在下丘脑的活动，并减少孤束核和背侧迷走神经复合体的脑干内的神经元活动。长期补充丁酸盐可预防饮食引起的肥胖、高胰岛素血症、高胆固醇血症和肝脂肪变性，这主要归因于食物摄入量的减少。丁酸盐还适度促进脂肪氧化和激活棕色脂肪组织（BAT），这从血浆甘油三酯衍生脂肪酸的利用率增加中可以看出。这种效应不是由于食物摄入量减少，而是通过增加交感神经流出到BAT来解释的。结论丁酸通过激活BAT，减少能量摄入，促进脂肪氧化，从而影响肠-脑神经回路，改善能量代谢。
Objective Butyrate exerts metabolic benefits in mice and humans, the underlying mechanisms being still unclear. We aimed to investigate the effect of butyrate on appetite and energy expenditure, and to what extent these two components contribute to the beneficial metabolic effects of butyrate.Design A cute effects of butyrate on appetite and its method of action were investigated in mice following an intragastric gavage or intravenous injection of butyrate. To study the contribution of satiety to the metabolic benefits of butyrate, mice were fed a high-fat diet with butyrate, and an additional pair-fed group was included. Mechanistic involvement of the gut-brain neural circuit was investigated in vagotomised mice.Results A cute oral, but not intravenous, butyrate administration decreased food intake, suppressed the activity of orexigenic neurons that express neuropeptide Y in the hypothalamus, and decreased neuronal activity within the nucleus tractus solitarius and dorsal vagal complex in the brainstem. Chronic butyrate supplementation prevented diet-induced obesity, hyperinsulinaemia, hypertriglyceridaemia and hepatic steatosis, largely attributed to a reduction in food intake. Butyrate also modestly promoted fat oxidation and activated brown adipose tissue (BAT), evident from increased utilisation of plasma triglyceride-derived fatty acids. This effect was not due to the reduced food intake, but explained by an increased sympathetic outflow to BAT. Subdiaphragmatic vagotomy abolished the effects of butyrate on food intake as well as the stimulation of metabolic activity in BAT.Conclusion Butyrate acts on the gut-brain neural circuit to improve energy metabolism via reducing energy intake and enhancing fat oxidation by activating BAT.