Adipokines and free fatty acids regulate insulin sensitivity by increasing microRNA-21 expression in human mature adipocytes.

Obesity is a global public health concern and may lead to a variety of complications. Previous studies have indicated that adipokines and energy-source materials contribute to obesity and obesity-associated insulin resistance. MicroRNAs (miRs) are endogenous 20- to 25-nucleotide non-coding RNAs associated with fat metabolism. It has been indicated that miR-21 is associated with adipogenesis and metabolic syndrome. In the present study, the expression of miR-21 in human mature adipocytes was analyzed using reverse transcription quantitative-polymerase chain reaction following treatment with adipokines, including tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, leptin, resistin and energy source materials, including free fatty acids (FFAs) and glucose. The current study demonstrated that the expression of miR-21 in human mature adipocytes was upregulated following treatment with TNF-alpha, IL-6, leptin, resistin and FFAs. However, low- and high-glucose did not have an effect on miR-21 expression. These results confirmed that TNF-a, IL-6, leptin, resistin and FFAs may contribute to obesity and obesity-associated insulin resistance via upregulating miR-21 in human mature adipocytes. Therefore, miR-21 may be a key regulatory factor of obesity and obesity-associated insulin resistance, and represents a potential therapeutic target for the treatment of these disorders.