小柯机器人

美国哥伦比亚大学Ivaylo I. Ivanov研究组发现，膳食糖诱导的微生物群失衡破坏免疫介导的对代谢综合征的保护。相关论文于2022年8月29日在线发表于国际学术期刊《细胞》。

研究人员发现，肠道微生物群通过诱导共生特异性Th17细胞来防止肥胖症、代谢综合征和糖尿病前期表型的发展。高脂肪、高糖饮食通过耗尽Th17诱导的微生物促进了代谢疾病，而共生Th17细胞的恢复修复了保护。微生物诱导的Th17细胞以IL-17依赖性的方式调节肠道上皮的脂质吸收，从而提供保护。饮食引起的保护性Th17细胞的丧失是由糖的存在所介导的。从高脂肪饮食中消除糖可以保护小鼠免于肥胖和代谢综合征，其方式依赖于共生特异性Th17细胞。糖和ILC3促进了Faecalibaculum rodentium的过度生长，这会取代诱导Th17的微生物群。

这些结果确定了构成代谢综合征风险的饮食和微生物群因素。这些结果还定义了膳食糖免疫致病性的微生物群依赖机制，并强调了饮食、微生物群和肠道免疫在调节代谢紊乱中的复杂互动。

据悉，人们对肠道微生物如何调节代谢综合征还不完全了解。

附：英文原文

Title: Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome

Author: Yoshinaga Kawano, Madeline Edwards, Yiming Huang, Angelina M. Bilate, Leandro P. Araujo, Takeshi Tanoue, Koji Atarashi, Mark S. Ladinsky, Steven L. Reiner, Harris H. Wang, Daniel Mucida, Kenya Honda, Ivaylo I. Ivanov

Issue&Volume: 2022-08-29

Abstract: How intestinal microbes regulate metabolic syndrome is incompletely understood. Weshow that intestinal microbiota protects against development of obesity, metabolicsyndrome, and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. High-fat,high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, andrecovery of commensal Th17 cells restored protection. Microbiota-induced Th17 cellsafforded protection by regulating lipid absorption across intestinal epithelium inan IL-17-dependent manner. Diet-induced loss of protective Th17 cells was mediatedby the presence of sugar. Eliminating sugar from high-fat diets protected mice fromobesity and metabolic syndrome in a manner dependent on commensal-specific Th17 cells.Sugar and ILC3 promoted outgrowth of Faecalibaculum rodentium that displaced Th17-inducing microbiota. These results define dietary and microbiotafactors posing risk for metabolic syndrome. They also define a microbiota-dependentmechanism for immuno-pathogenicity of dietary sugar and highlight an elaborate interactionbetween diet, microbiota, and intestinal immunity in regulation of metabolic disorders.

DOI: 10.1016/j.cell.2022.08.005

Source: https://www.cell.com/cell/fulltext/S0092-8674(22)00992-8