The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.
The gut microbiota suppresses insulin-mediated fat accumulation via the short-chain fatty acid receptor GPR43.
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肠道菌群通过短链脂肪酸受体GPR43抑制胰岛素介导的脂肪积累。
DOI：
10.1038/ncomms2852
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发表时间：
2013
影响因子：
16.6
通讯作者：
中科院分区：
文献类型：
--
作者：
肠道菌群影响宿主的营养获取和能量调节，并影响肥胖、胰岛素抵抗和糖尿病的发生。在摄食过程中，肠道微生物产生短链脂肪酸，这是宿主重要的能量来源。在这里，我们表明短链脂肪酸受体GPR43将肠道微生物群的代谢活动与宿主体内能量平衡联系起来。我们证明GPR43缺乏的小鼠在正常饮食中肥胖，而在脂肪组织中特异性表达GPR43的小鼠即使在喂食高脂肪饮食时也保持苗条。在无菌条件下饲养或用抗生素治疗后，两种类型的小鼠都有正常的表型。我们进一步表明，短链脂肪酸介导的GPR43激活抑制脂肪细胞中的胰岛素信号，从而抑制脂肪组织中的脂肪积累，促进其他组织中未合并脂质和葡萄糖的代谢。这些发现表明GPR43是过量膳食能量的传感器，从而控制机体能量利用，同时维持代谢平衡。肠道微生物群产生代谢物，如短链脂肪酸（SCFAs），它可以影响肥胖的发展。在这里，Kimura等人表明，SCFAs通过受体GPR43起作用，GPR43作为过量饮食能量的传感器，控制身体能量利用和代谢平衡。
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. The gut microbiota produces metabolites such as short-chain fatty acids (SCFAs), which can influence the development of obesity. Here Kimura et al. show that SCFAs act via the receptor GPR43, which acts as a sensor for excessive dietary energy and controls body energy utilization as well as metabolic homoeostasis.
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影响因子：
29
作者：
Hatori M;Vollmers C;Zarrinpar A;DiTacchio L;Bushong EA;Gill S;Leblanc M;Chaix A;Joens M;Fitzpatrick JA;Ellisman MH;Panda S
通讯作者：
Panda S
DOI：
10.1152/ajpendo.00229.2010
发表时间：
2011-01-01
影响因子：
5.1
作者：
Bjursell, Mikael;Admyre, Therese;Bohlooly-Y, Mohammad
通讯作者：
Bohlooly-Y, Mohammad
影响因子：
4.8
作者：
Brown, AJ;Goldsworthy, SM;Dowell, SJ
通讯作者：
Dowell, SJ
影响因子：
4.2
作者：
HOVERSTAD, T;MIDTVEDT, T
通讯作者：
MIDTVEDT, T
影响因子：
2.2
作者：
De Gregoris, Tristano Bacchetti;Aldred, Nick;Burgess, J. Grant
通讯作者：
Burgess, J. Grant