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J Clin Gastroenterol. 2010 Sep;44 Suppl 1:S16-8. doi: 10.1097/MCG.0b013e3181dd8b64.

Obesity, metabolic syndrome, and microbiota: multiple interactions.

Author information

  • Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Austria. herbert.tilg@i-med.ac.at

Abstract

The incredible number and diversity of microorganisms in the human gastrointestinal tract represent a very diverse set of features, which support the host in important functions such as digestion of complex carbohydrates. Conventionalization of germ-free mice with a normal gut microbiota harvested from the intestine of conventionally raised mice results in weight gain and obesity. Development of obesity in genetically or diet-induced obese mice is associated with dramatic changes in the composition and metabolic function of the microbiota. This trait is transmissible as colonization of germ-free mice with an "obese-gut-derived" microflora results in a much greater increase in total body fat and leads to obesity. The first studies in obese and lean twins suggest that a core gut microbiome exists, and that obese individuals exhibit reduced diversity and an altered representation of metabolic pathways in their microbiota. Diet may have a fundamental effect on the composition of our microbiota. Early studies highlight the importance for specific diets such as a high-fat diet, which efficiently and very rapidly (within a single day) modulates the gut microbiome. The innate immune system might influence the metabolic syndrome and obesity, as mice deficient in Toll-like receptor 5 develop hyperphagia, become obese and insulin resistant. Importantly, transmission of the microbiota from these mice to healthy mice results in features of the metabolic syndrome. Available data suggest that the microbiota might play a role in the development of metabolic syndrome and obesity.

PMID:
20535027
[PubMed - indexed for MEDLINE]
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