| dc.description.abstract | Obesity causes a wide variety of metabolic diseases including fatty liver disease and diabetes. Mechanistically, obesity-associated inflammation has been implicated as a key factor in the development of fat deposition, insulin resistance, and metabolic dysregulation. As a member of the G-protein coupled receptor families, adenosine 2A receptor (A2AR) is anti-inflammatory. However, little is known about nutritional regulation of A2AR as it relates to insulin resistance.
In the present study, the expression of A2AR in liver and adipose tissue was examined in wild type (WT) C57BL/6J mice upon feeding a high-fat diet (HFD) or a low-fat diet (LFD). Also, both A2AR-deficient mice and WT mice were fed an HFD for 12 weeks to examine the involvement of A2AR in diet-induced inflammation and insulin resistance. Lastly, the effects of major macronutrients, i.e. glucose and palmitate, on the inflammatory responses were examined in adipocytes and macrophages, either from WT or A2AR-deficient background.
HFD increased the expression of A2AR in liver and adipose tissue, accompanied with obesity-related inflammation and insulin resistance. It appeared to be a defensive response, which may help protect against inflammatory damage. Nutrients had direct effects on A2AR expression in both adipocytes and macrophages, which indicated A2AR had protection effects on inflammation. When comparing with HFD-fed WT mice, HFD-fed A2AR-deficient mice displayed a significant increase in the severity of inflammation and insulin resistance. | en |
