Butyrate improves insulin sensitivity and increases energy expenditure in mice.
Butyrate improves insulin sensitivity and increases energy expenditure in mice.
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作者：
Gao Z;Yin J;Zhang J;Ward RE;Martin RJ;Lefevre M;Cefalu WT;Ye J
我们研究了丁酸（一种在大肠中发酵形成的短链脂肪酸）在高脂肪饮食小鼠胰岛素敏感性调节中的作用。在饮食肥胖的C57BL/6J小鼠中，在高脂肪饮食中以5% wt/wt的比例添加丁酸钠。通过胰岛素耐量试验和胰岛素抵抗的稳态模型评估来检查胰岛素敏感性。在代谢室中监测能量代谢。研究了小鼠棕色脂肪细胞和骨骼肌的线粒体功能。在高脂肪饮食中，补充丁酸盐可以防止C57BL/6小鼠胰岛素抵抗和肥胖的发生。治疗小鼠的空腹血糖、空腹胰岛素和胰岛素耐量均保持不变。在不减少食物摄入量的情况下，体脂含量保持在10%。适应性产热和脂肪酸氧化增强。骨骼肌和棕色脂肪的线粒体功能和生物发生增加。I型纤维在骨骼肌中富集。过氧化物酶体增殖物激活受体-γ共激活因子-1α在mRNA和蛋白水平上表达升高。AMP激酶和p38活性升高。在肥胖小鼠中，补充丁酸盐导致胰岛素敏感性的增加和肥胖的减少。饲粮中添加丁酸盐可预防和治疗小鼠饮食性胰岛素抵抗。丁酸盐的作用机制与促进能量消耗和诱导线粒体功能有关。
We examined the role of butyric acid, a short-chain fatty acid formed by fermentation in the large intestine, in the regulation of insulin sensitivity in mice fed a high-fat diet. In dietary-obese C57BL/6J mice, sodium butyrate was administrated through diet supplementation at 5% wt/wt in the high-fat diet. Insulin sensitivity was examined with insulin tolerance testing and homeostasis model assessment for insulin resistance. Energy metabolism was monitored in a metabolic chamber. Mitochondrial function was investigated in brown adipocytes and skeletal muscle in the mice. On the high-fat diet, supplementation of butyrate prevented development of insulin resistance and obesity in C57BL/6 mice. Fasting blood glucose, fasting insulin, and insulin tolerance were all preserved in the treated mice. Body fat content was maintained at 10% without a reduction in food intake. Adaptive thermogenesis and fatty acid oxidation were enhanced. An increase in mitochondrial function and biogenesis was observed in skeletal muscle and brown fat. The type I fiber was enriched in skeletal muscle. Peroxisome proliferator–activated receptor-γ coactivator-1α expression was elevated at mRNA and protein levels. AMP kinase and p38 activities were elevated. In the obese mice, supplementation of butyrate led to an increase in insulin sensitivity and a reduction in adiposity. Dietary supplementation of butyrate can prevent and treat diet-induced insulin resistance in mouse. The mechanism of butyrate action is related to promotion of energy expenditure and induction of mitochondria function.