脂肪组织
肠道菌群
能量稳态
胰岛素抵抗
脂肪酸
生物
短链脂肪酸
平衡
内分泌学
营养感应
胰岛素
新陈代谢
葡萄糖稳态
内科学
肥胖
生物化学
信号转导
医学
丁酸盐
发酵
作者
Ikuo Kimura,Kentaro Ozawa,Daisuke Inoue,Teruhiko Imamura,Kumi Kimura,Takeshi Maeda,Kazuya Terasawa,Daiji Kashihara,Keihachiro Hirano,Taeko Tani,Tomoyuki Takahashi,Satoshi Miyauchi,Go Shioi,Hiroshi Inoue,Gozoh Tsujimoto
摘要
The gut microbiota affects nutrient acquisition and energy regulation of the host, and can influence the development of obesity, insulin resistance, and diabetes. During feeding, gut microbes produce short-chain fatty acids, which are important energy sources for the host. Here we show that the short-chain fatty acid receptor GPR43 links the metabolic activity of the gut microbiota with host body energy homoeostasis. We demonstrate that GPR43-deficient mice are obese on a normal diet, whereas mice overexpressing GPR43 specifically in adipose tissue remain lean even when fed a high-fat diet. Raised under germ-free conditions or after treatment with antibiotics, both types of mice have a normal phenotype. We further show that short-chain fatty acid-mediated activation of GPR43 suppresses insulin signalling in adipocytes, which inhibits fat accumulation in adipose tissue and promotes the metabolism of unincorporated lipids and glucose in other tissues. These findings establish GPR43 as a sensor for excessive dietary energy, thereby controlling body energy utilization while maintaining metabolic homoeostasis.
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