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儿童肠道微生物组产生的短链脂肪酸与肥胖。

Gut microbiome production of short-chain fatty acids and obesity in children.

机构信息

Departamento de Genética y Biología Molecular, Centro de Investigación y de Estudios Avanzados del IPN, Unidad Zacatenco, Av. Instituto Politécnico Nacional 2508, 07360, Ciudad de México, Mexico.

Departamento de Farmacología, Centro de Investigación y de Estudios Avanzados del IPN, Unidad Zacatenco, Av. Instituto Politécnico Nacional 2508, 07360, Ciudad de México, Mexico.

出版信息

Eur J Clin Microbiol Infect Dis. 2018 Apr;37(4):621-625. doi: 10.1007/s10096-017-3143-0. Epub 2017 Dec 2.

Abstract

Obesity has been a worldwide multifactorial epidemic malady for the last 2 decades. Changes in gut microbiota composition and its metabolites - short-chain fatty acids (SCFAs) - have been associated with obesity. Recent evidence suggests that SCFAs made by the gut microbiota may regulate directly or indirectly physiological and pathological processes in relation to obesity. We review the influence of gut microbiota in energy, glucose, and lipid homeostasis control via their metabolites. Gut microbial disturbances in obese children may have a role in their metabolism. At first glance, excessive short-chain fatty acids produced by a particular gut microbiota represent an additional energy source, and should cause an imbalance in energy regulation, contributing to obesity. However, simultaneously, SCFA participates in glucose-stimulated insulin secretion from the pancreatic β-cells through interaction with the FFA2 and FFA3 receptors, and release of peptide hormones which control appetite. This apparent contradictory situation may indicate the involvement of additional particular bacteria or bacterial components or metabolites that may trigger regulatory cascades by interaction with some G-protein-coupled membrane receptors.

摘要

在过去的 20 年中,肥胖已成为一种全球性的多因素流行疾病。肠道微生物群落组成及其代谢物——短链脂肪酸(SCFAs)的变化与肥胖有关。最近的证据表明,肠道微生物群产生的 SCFAs 可能直接或间接地调节与肥胖相关的生理和病理过程。我们综述了肠道微生物群通过其代谢物对能量、葡萄糖和脂质稳态控制的影响。肥胖儿童的肠道微生物紊乱可能在其代谢中起作用。乍一看,特定肠道微生物群产生的过多短链脂肪酸代表了额外的能量来源,并且应该导致能量调节失衡,导致肥胖。然而,同时,SCFA 通过与 FFA2 和 FFA3 受体相互作用以及控制食欲的肽激素的释放,参与胰腺β细胞的葡萄糖刺激胰岛素分泌。这种明显矛盾的情况可能表明涉及其他特定细菌或细菌成分或代谢物,它们可能通过与某些 G 蛋白偶联膜受体相互作用触发调节级联反应。

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