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Microbiota-induced obesity requires farnesoid X receptor

Artikel i vetenskaplig tidskrift
Författare Ava Parseus
Nina Sommer
Felix Sommer
Robert Caesar
Antonio Molinaro
Marcus Ståhlman
Thomas U. Greiner
Rosie Perkins
Fredrik Bäckhed
Publicerad i Gut
Volym 66
Nummer/häfte 3
Sidor 429-437
ISSN 0017-5749
Publiceringsår 2017
Publicerad vid Wallenberglaboratoriet
Institutionen för medicin, avdelningen för molekylär och klinisk medicin
Sidor 429-437
Språk en
Ämnesord bile-acid metabolism, diet-induced obesity, fatty liver-disease, gut, microbiota, insulin-resistance, nuclear receptor, vldl receptor, fxr, extraction, mouse, Gastroenterology & Hepatology, dtvedt t, 1974, american journal of clinical nutrition, v27, p1341, lch j, 1957, journal of biological chemistry, v226, p497
Ämneskategorier Endokrinologi och diabetes, Kardiologi

Sammanfattning

Objective The gut microbiota has been implicated as an environmental factor that modulates obesity, and recent evidence suggests that microbiota-mediated changes in bile acid profiles and signalling through the bile acid nuclear receptor farnesoid X receptor (FXR) contribute to impaired host metabolism. Here we investigated if the gut microbiota modulates obesity and associated phenotypes through FXR. Design We fed germ-free (GF) and conventionally raised (CONV-R) wild-type and Fxr(-/-) mice a high-fat diet (HFD) for 10 weeks. We monitored weight gain and glucose metabolism and analysed the gut microbiota and bile acid composition, beta-cell mass, accumulation of macrophages in adipose tissue, liver steatosis, and expression of target genes in adipose tissue and liver. We also transferred the microbiota of wild-type and Fxr(-) deficient mice to GF wild-type mice. Results The gut microbiota promoted weight gain and hepatic steatosis in an FXR-dependent manner, and the bile acid profiles and composition of faecal microbiota differed between Fxr(-/-) and wild-type mice. The obese phenotype in colonised wild-type mice was associated with increased beta-cell mass, increased adipose inflammation, increased steatosis and expression of genes involved in lipid uptake. By transferring the caecal microbiota from HFD-fed Fxr(-/-) and wild-type mice into GF mice, we showed that the obesity phenotype was transferable. Conclusions Our results indicate that the gut microbiota promotes diet-induced obesity and associated phenotypes through FXR, and that FXR may contribute to increased adiposity by altering the microbiota composition.

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