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Intestinal microbiota (IM) plays a role in the development of obesity and its associated low-grade inflammation. Bacterial colonization of the gastrointestinal tract of germ-free mice (without microbiota) increases by 60% their fat mass, alters their fasting glucose and insulin levels, triples their hepatic triglycerides and induces adipocyte hypertrophy. IM favors fat storage in adipocytes through the inhibition of Fiaf (Fasting-Induced Adipocyte Factor), an inhibitor of lipoprotein lipase. Compa-red with normal weight subjects, the IM from obese exhibits a higher proportion of Firmicutes/Bacteroidetes and is more efficient in extracting energy from foodstuffs. The loss of bodyweight by a hypocaloric diet reverts the proportion of bacteria to that of lean subjects. The intake of a high fat diet also alters the IM, affecting intes-tinal barrier function and favoring endotoxinemia. These events increase oxidative and pro-inflammatory processes in plasma and peripheral tissues and increment the risk of insulin resistance. Such events are reverted by the administration of pre-biotics which stimulate the growth of Bifidobacterium and Lactobacillus species in the colon, reestablishing the gut homeostasis. Interestingly, products resulting from the fermentation of prebiotics stimulate the differentiation of enteroendocrine cells and the release of glucagon-like peptide 1 and peptide YY, that have insulin-like and anorexigenic activities, thus contributing to body weight equilibrium. (Rev Med Chile 2010; 138: 1020-1027).

La microbiota intestinal: Un nuevo actor en el desarrollo de la obesidad