Metabolism Xagena

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Xagena Newsletter
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Gut microbiota-derived lipopolysaccharide is involved in the development of obesity

The composition of the gut microbiota and excessive ingestion of high-fat diets ( HFD ) are considered to be important factors for development of obesity.

Researchers have described a coherent mechanism of action for the development of obesity, which involves the composition of gut microbiota, high-fat diet, low-grade inflammation, expression of fat translocase and scavenger receptor CD36, and the scavenger receptor class B type 1 ( SR-BI ).

SR-BI binds to both lipids and lipopolysaccharide ( LPS ) from Gram-negative bacteria, which may promote incorporation of lipopolysaccharide in chylomicrons ( CMs ). These chylomicrons are transported via lymph to the circulation, where lipopolysaccharide is transferred to other lipoproteins by translocases, preferentially to HDL.

Lipopolysaccharide increases the SR-BI binding, transcytosis of lipoproteins over the endothelial barrier,and endocytosis in adipocytes. Especially large size adipocytes with high metabolic activity absorb LPS-rich lipoproteins.

In addition, macrophages in adipose tissue internalize LPS-lipoproteins. This may contribute to the polarization from M2 to M1 phenotype, which is a consequence of increased lipopolysaccharide delivery into the tissue during hypertrophy.

In conclusion, evidence suggests that lipopolysaccharide is involved in the development of obesity as a direct targeting molecule for lipid delivery and storage in adipose tissue. ( Xagena )

Hersoug L-G et al, Obesity Reviews 2016; 17: 297–312