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Fig. 2 | Genome Medicine

Fig. 2

From: Impact of the gut microbiota on inflammation, obesity, and metabolic disease

Fig. 2

Metabolic and immune interactions between gut microbes and the host in obesity and the metabolic syndrome. The gut microbiota is involved in a molecular crosstalk with the host that modulates host physiology, metabolism, and inflammatory status. In particular, the gut microbiota participates in the physiology and motility of the digestive tract and in the digestion of polysaccharides, which directly influences host energy availability. The gut microbiota inhibits fasting-induced adipose factor (FIAF) in the intestine and monophosphate activated protein kinase (AMPK) in several organs such as the brain and muscle, which results in increasing fat deposition. The short-chain fatty acids (SCFAs) produced by bacteria from polysaccharides interact with G protein-coupled receptors (GPCRs; GPR41, GPR43, and GPR109A), which stimulates gut motility and host immunity. The gut microbiota also contributes to fat deposition through the regulation of the farnesoid X receptor (FXR), the bile acid receptor responsible for the regulation of bile acid synthesis and hepatic triglyceride accumulation. The gut microbiota converts choline to trimethylamine, thus influencing the bioavailability of choline for host use and indirectly affecting phosphatidylcholine production and hepatic triglyceride transport by very-low-density lipoproteins (VLDLs)

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