某种肠道细菌
产热
葡萄糖稳态
褐色脂肪组织
脂肪组织
分泌物
能量稳态
胰高血糖素样肽-1
肠道菌群
内分泌学
内科学
受体
生物
糖尿病
胰岛素抵抗
化学
生物化学
2型糖尿病
医学
作者
Hye-Kyung Yoon,Chung Hwan Cho,Myeong Sik Yun,Sung Jae Jang,Hyun Ju You,Jun Hyeong Kim,Dohyun Han,Kwang Hyun,Seol Ju Moon,Kiuk Lee,Yeon Ji Kim,Sung Joon Lee,Tae Wook Nam,Gwang Pyo Ko
出处
期刊:Nature microbiology
日期:2021-04-05
卷期号:6 (5): 563-573
被引量:249
标识
DOI:10.1038/s41564-021-00880-5
摘要
The gut microbiota, which includes Akkermansia muciniphila, is known to modulate energy metabolism, glucose tolerance, immune system maturation and function in humans1-4. Although A. muciniphila is correlated with metabolic diseases and its beneficial causal effects were reported on host metabolism5-8, the molecular mechanisms involved have not been identified. Here, we report that A. muciniphila increases thermogenesis and glucagon-like peptide-1 (GLP-1) secretion in high-fat-diet (HFD)-induced C57BL/6J mice by induction of uncoupling protein 1 in brown adipose tissue and systemic GLP-1 secretion. We apply fast protein liquid chromatography and liquid chromatography coupled to mass spectrophotometry analysis to identify an 84 kDa protein, named P9, that is secreted by A. muciniphila. Using L cells and mice fed on an HFD, we show that purified P9 alone is sufficient to induce GLP-1 secretion and brown adipose tissue thermogenesis. Using ligand-receptor capture analysis, we find that P9 interacts with intercellular adhesion molecule 2 (ICAM-2). Interleukin-6 deficiency abrogates the effects of P9 in glucose homeostasis and downregulates ICAM-2 expression. Our results show that the interactions between P9 and ICAM-2 could be targeted by therapeutics for metabolic diseases.
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