Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome.
Microbiota imbalance induced by dietary sugar disrupts immune-mediated protection from metabolic syndrome.
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DOI：
10.1016/j.cell.2022.08.005
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发表时间：
2022-09-15
期刊：
影响因子：
64.5
通讯作者：
Ivanov, Ivaylo I.
中科院分区：
文献类型：
--
作者：
Kawano, Yoshinaga;Edwards, Madeline;Huang, Yiming;Bilate, Angelina M.;Araujo, Leandro P.;Tanoue, Takeshi;Atarashi, Koji;Ladinsky, Mark S.;Reiner, Steven L.;Wang, Harris H.;Mucida, Daniel;Honda, Kenya;Ivanov, Ivaylo I.
肠道微生物如何调节代谢综合征还不完全清楚。我们发现肠道微生物群通过诱导肠道特异性Th 17细胞来防止肥胖、代谢综合征和糖尿病前期表型的发展。高脂肪、高糖饮食通过消耗Th 17诱导微生物促进代谢疾病，而骨髓Th 17细胞的恢复恢复了保护作用。微生物群诱导的Th 17细胞通过以IL-17依赖性方式调节肠上皮的脂质吸收来提供保护。饮食诱导的保护性Th 17细胞的丧失是由糖的存在介导的。从高脂饮食中排除糖可以保护小鼠免受肥胖和代谢综合征的影响，这依赖于特定的Th 17细胞。糖和ILC 3促进了啮齿类粪杆菌的生长，取代了Th 17诱导的微生物群。这些结果定义了构成代谢综合征风险的饮食和微生物群因素。他们还定义了饮食糖的免疫致病性的微生物群依赖性机制，并强调了饮食，微生物群和肠道免疫之间在代谢紊乱调节中的复杂相互作用。小鼠饮食中的糖通过扰乱肠道微生物平衡和驱动调节肠上皮细胞脂质吸收的Th 17细胞的损失来促进代谢疾病。
How intestinal microbes regulate metabolic syndrome is incompletely understood. We show that intestinal microbiota protects against development of obesity, metabolic syndrome and pre-diabetic phenotypes by inducing commensal-specific Th17 cells. High-fat, high-sugar diet promoted metabolic disease by depleting Th17-inducing microbes, and recovery of commensal Th17 cells restored protection. Microbiota-induced Th17 cells afforded protection by regulating lipid absorption across intestinal epithelium in an IL-17-dependent manner. Diet-induced loss of protective Th17 cells was mediated by the presence of sugar. Eliminating sugar from high-fat diet protected mice from obesity 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 microbiota factors posing risk for metabolic syndrome. They also define a microbiota-dependent mechanism for immuno-pathogenicity of dietary sugar and highlight an elaborate interaction between diet, microbiota, and intestinal immunity in regulation of metabolic disorders. Sugar in mouse diets promotes metabolic disease by upsetting the gut microbial balance and driving loss of the Th17 cells that regulate lipid absorption by the intestinal epithelium.
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影响因子：
7.7
作者：
Hajri, Tahar;Hall, Angela M.;Abumrad, Nada A.
通讯作者：
Abumrad, Nada A.
影响因子：
7.7
作者：
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通讯作者：
Guerre-Millo, Michele
膳食脂肪对肠道炎症的调节。
影响因子：
7.3
作者：
Basson AR;Chen C;Sagl F;Trotter A;Bederman I;Gomez-Nguyen A;Sundrud MS;Ilic S;Cominelli F;Rodriguez-Palacios A
通讯作者：
Rodriguez-Palacios A
影响因子：
3.7
作者：
Buttet M;Poirier H;Traynard V;Gaire K;Tran TT;Sundaresan S;Besnard P;Abumrad NA;Niot I
通讯作者：
Niot I
DOI：
10.1152/ajpendo.2001.281.5.e916
发表时间：
2001-11-01
影响因子：
5.1
作者：
Chen, M;Yang, YK;Harmon, CM
通讯作者：
Harmon, CM