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首页> 外文期刊>Cell metabolism >Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice
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Microbiota-Dependent Hepatic Lipogenesis Mediated by Stearoyl CoA Desaturase 1 (SCD1) Promotes Metabolic Syndrome in TLR5-Deficient Mice

机译：硬脂酰辅酶A去饱和酶1（SCD1）介导的微生物群依赖的肝脏脂肪生成促进TLR5缺陷小鼠的代谢综合征。

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摘要

The gut microbiota plays a key role in host metabolism. Toll-like receptor 5 (TLR5), a flagellin receptor, is required for gut microbiota homeostasis. Accordingly, TLR5-deficient (T5KO) mice are prone to develop microbiota-dependent metabolic syndrome. Here we observed that T5KO mice display elevated neutral lipids with a compositional increase of oleate [C18:1 (n9)] relative to wild-type littermates. Increased oleate contribution to hepatic lipids and liver SCD1 expression were both microbiota dependent. Analysis of short-chain fatty acids (SCFAs) and C-13-acetate label incorporation revealed elevated SCFA in ceca and hepatic portal blood and increased liver de novo lipogenesis in T5KO mice. Dietary SCFAs further aggravated metabolic syndrome in T5KO mice. Deletion of hepatic SCD1 not only prevented hepatic neutral lipid oleate enrichment but also ameliorated metabolic syndrome in T5KO mice. Collectively, these results underscore the key role of the gut microbiota-liver axis in the pathogenesis of metabolic diseases.
机译：肠道菌群在宿主代谢中起关键作用。鞭毛蛋白受体Toll样受体5（TLR5）是肠道菌群稳态的必需物质。因此，缺乏TLR5的（T5KO）小鼠容易出现微生物群依赖性代谢综合征。在这里，我们观察到T5KO小鼠相对于野生型同窝小鼠显示出升高的中性脂质，且油酸酯的组成增加[C18：1（n9）]。油酸对肝脂质和肝脏SCD1表达的贡献均与微生物群有关。对短链脂肪酸（SCFA）和C-13-乙酸盐标记掺入的分析显示，盲肠和肝门静脉血中SCFA升高，在T5KO小鼠中肝脏新生脂肪生成增加。饮食中的SCFA进一步加重了T5KO小鼠的代谢综合症。肝SCD1的删除不仅阻止了肝中性脂质油酸盐的富集，而且改善了T5KO小鼠的代谢综合征。总体而言，这些结果强调了肠道微生物群-肝轴在代谢性疾病发病机理中的关键作用。

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