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)‑α, 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‑α, 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‑α, 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.