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