Endothelium dysfunction has been understood primarily in terms of abnormal vasomotor function, which plays an important role in the pathogenesis of diabetes and chronic diabetic complications. However, it has not been fully studied that the endothelium may regulate metabolism itself. The response gene to complement 32 (RGC-32) has be considered as an angiogenic inhibitor in the context of endothelial cells. We found that RGC-32 was induced by high fat diet in vivo and by glucose or insulin in endothelial cells, and then we set out to investigate the role of endothelial RGC-32 in metabolism. DNA array analysis and qPCR results showed that glutamine-fructose-6-phosphate aminotransferase [isomerizing] 1 (GFPT1), solute carrier family 2 (facilitated glucose transporter), member 12 (SLC2A12, GLUT12) and glucagon-like peptide 2 receptor (GLP2R) may be among possible glucose metabolism related downstream genes of RGC-32. Additionally, in the mice with endothelial specific over-expressed RGC-32, the disposal of carbohydrate was improved without changing insulin sensitivity when mice were faced with high fat diet challenges. Taken together, our findings suggest that RGC-32 in the endothelial cells regulates glucose metabolism related genes and subsequent helps to maintain the homeostasis of blood glucose.
Keywords: The response gene to complement 32; endothelial cells; glucose homeostasis.