Bacterial lipopolysaccharides and metabolic diseases

被引:1
作者
Burcelin, Remy [1 ]
Chabo, Chantal [1 ]
Luche, Elodie [1 ]
Serino, Matteo [1 ]
Corthier, G. [2 ]
机构
[1] Hop Rangueil, Inserm U858 Eq2, Inst Med Mol Rangueil, BP 84225, F-31432 Toulouse 4, France
[2] Inra Micalis CRJ, F-78350 Jouy En Josas, France
来源
CAHIERS DE NUTRITION ET DE DIETETIQUE | 2010年 / 45卷 / 03期
关键词
Diabetes; Obesity; Inflammation; Lipopolysaccharides; Intestinal microbiota;
D O I
10.1016/j.cnd.2010.03.001
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
The rapid outbreak of metabolic diseases cannot be explained solely by the role of genetic mutations. Conversely, changes in feeding habits, which occurred simultaneously to the occurrence of the metabolic diseases, could certainly be the leading causes. Recent evidences from the literature proposed that intestinal microbiota could be the direct consequence of changes induced by the increased proportion of fat and the reduced proportion of fibers in the diet. A new intestinal microbiota ecology has emerged consequently to the change in feeding habits. The use of germ free mice has allowed the recent demonstration of the functional role of intestinal microbiota on the development of metabolic diseases. The colonization of axenic germ free mice by the means of conventional microbiota has demonstrated that metabolic diseases originate from a change in microbial ecology. Furthermore, we showed that intestinal microbiota could be at the origin of the low tone inflammation which characterizes diabetes and obesity. Indeed, lipopolysaccharides issue from Gram-negative bacteria increased in the blood in response to a fat-enriched diet and are at the onset of insulin resistance and adipose hyperplasia and hypertrophy. Therefore, nutritional approaches based on pre-and probiotic strategies could certainly, in the near future, restore this microbial ecology and slow down the dramatic development of metabolic diseases. (C) 2010 Published by Elsevier Masson SAS on behalf of Societe francaise de nutrition.
引用
收藏
页码:114 / 121
页数:8
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