Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic syndrome is a group of obesity-related metabolic abnormalities that increase an individual's risk of developing type 2 diabetes and cardiovascular disease. Here, we show that mice genetically deficient in Toll-like receptor 5 (TLR5), a component of the innate immune system that is expressed in the gut mucosa and that helps defend against infection, exhibit hyperphagia and develop hallmark features of metabolic syndrome, including hyperlipidemia, hypertension, insulin resistance, and increased adiposity. These metabolic changes correlated with changes in the composition of the gut microbiota, and transfer of the gut microbiota from TLR5-deficient mice to wild-type germ-free mice conferred many features of metabolic syndrome to the recipients. Food restriction prevented obesity, but not insulin resistance, in the TLR5-deficient mice. These results support the emerging view that the gut microbiota contributes to metabolic disease and suggest that malfunction of the innate immune system may promote the development of metabolic syndrome.
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PMID:Metabolic syndrome and altered gut microbiota in mice lacking Toll-like receptor 5. 2148 25

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.
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PMID:Obesity, metabolic syndrome, and microbiota: multiple interactions. 2053 27