Obesity and Type II diabetes mellitus: Is resistin the link?

There has been much effort recently to explore the role of adipocytokines in the interaction between adipose tissue, inflammation, and immunity. Tumor necrosis factor-alpha, interleukin-6, resistin, and many other adipocytokines are the soluble mediators derived mainly from adipocytes (fat cells). They are known to influence insulin sensitivity and glucose metabolism profoundly, thus providing a molecular link between increased adiposity and insulin resistance (IR). Resistin, an adipocytokine, is a member of a class of cysteine-rich proteins, collectively termed resistin-like molecules. They were initially discovered in rodents. It is present in gross visceral fat deposits and is released by adipocytes in humans. Owing to the regional variation in the expression of resistin mRNA and protein levels in humans, the highest levels have been noted in the abdominal depot. It is interesting to note that resistin also gets released from infiltrating white blood cells subsequent to subclinical chronic low-grade inflammatory response, accompanying obesity. This convergence of adipocyte and macrophage function in obese Type II diabetics has paved its role in molecular linkage of obesity, inflammation and metabolic syndrome (MetS) risk. Resistin, being a pro-inflammatory adiopokine, contributes to atherosclerosis. High serum resistin levels have been found, although with some inconsistencies, in cardiovascular patients, labeling it as a cardiovascular disease (CVD) marker, to predict incident cardiovascular events. Both IR and inflammation are the pathogenic factors contributing to increased risk of CVD, associated with diabetes, thus tagging resistin as a potential MetS marker. In conclusion, resistin is a fascinating new hormone awaiting further research in the obesity – IR – diabetes – MetS link.

Keywords

Adipocytokines - diabetes - obesity - resistin

Publication History

Article published online:
08 June 2022