Intestinal microbiota in inflammation and insulin resistance: relevance to humans

被引:61
作者
De Bandt, Jean-Pascal [1 ,3 ]
Waligora-Dupriet, Anne-Judith [2 ]
Butel, Marie-Jose [2 ]
机构
[1] Fac Sci Pharmaceut Paris Descartes, Dept Biol Expt Metab & Clin, EA4466, F-75270 Paris 06, France
[2] Fac Sci Pharmaceut Paris Descartes, Dept Perinatal, EA4065, F-75270 Paris 06, France
[3] Cochin Broca Hotel Dieu, APHP, Paris, France
关键词
gut microbiota; gut permeability; lipopolysaccharide; obesity; HUMAN GUT MICROBIOTA; DIET-INDUCED OBESITY; INDUCED HEPATIC STEATOSIS; ENDOTOXIN LEVELS; ADIPOSE-TISSUE; WEIGHT-LOSS; LINKS; MICE; PROBIOTICS; RESPONSES;
D O I
10.1097/MCO.0b013e328347924a
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Purpose of review The gut microbiota is a very complex ecosystem which interacts extensively with the host, influencing multiple metabolic and physiological functions. Several diseases have been shown to be associated with specific alterations in gut microbiota. It is more and more underscored as playing a major role in the development of insulin resistance and inflammation associated with excess weight gain. Recent findings Recent studies in obese patients have shown perturbations in gut microbiota with a weight gain-associated increase in the Firmicutes/Bacteroidetes ratio ameliorated by various attempts at inducing weight loss. Summary Intestinal microbiota may contribute to the development of inflammation and insulin resistance by two main mechanisms. First, gut microbiota might facilitate energy harvest from the gut leading via perturbation in energy homeostasis to fat deposition and increased adipokine production and plasma free fatty acid levels both contributing to insulin resistance and inflammation. Alternatively, it can initiate an inflammatory process either originating from the intestine or generated at the peripheral level via endotoxin leakage into the blood from the intestine, both leading secondarily to insulin resistance.
引用
收藏
页码:334 / 340
页数:7
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