PLASMA ZINC ASSOCIATION WITH microRNA PROFILE IN WOMEN WITH INSULIN RESISTANCE
microRNA, insulin resistance, zinc, overweight, diabetes.
Zinc plays an essential role in insulin metabolism, and alterations in the signaling pathway of this hormone can trigger a deficiency of this mineral. Insulin resistance (IR) is the primary cause of type 2 diabetes development. In this context, microRNAs (miRs) play an important role in regulating multiple processes, including insulin signaling pathways and glucose metabolism. Excess or deficiency of nutrients can modulate the expression of miRs and, thus, influence the risk of developing diseases. However, the specific role of miRs related to glucose metabolism in the zinc status is not clear. Therefore, the aim of this study is to evaluate the association of miRs related to glucose homeostasis (miR-191-5p, miR-188-5p, miR-145-5p, and miR-143-3p) with plasma zinc concentration in women with IR. This comparative cross-sectional study was conducted with adult women with a Body Mass Index (BMI) ≥ 25 kg/m2. IR classification was performed according to the Brazilian Diabetes Society Guidelines, based on the criteria proposed by Stern (2005). Anthropometric assessment, plasma zinc concentration, miR expression, and biochemical profile were conducted. This study included a sample of 50 women diagnosed with IR, with only 6% diagnosed with zinc deficiency. After dividing plasma zinc into tertiles, a significant difference was observed in the concentration of LPS (p=0.050) - T3 higher than T1 and T2 - and IL-1β - T3 higher than T1. Furthermore, a positive correlation was observed between plasma zinc and serum HDL-c concentration (rho=0.279; p=0.050), and a negative correlation with miR-191-5p (rho= -0.428; p=0.002), miR-145-5p (rho=-0.384; p=0.006), and miR-143-3p (rho=-0.357; p=0.011). Therefore, this study identified that plasma zinc showed an inverse correlation with three miRs related to glucose homeostasis (miR-191-5p, miR-145-5p, and miR-143-3p) in women with IR, indicating a possible epigenomic interaction of zinc in the biological processes involved in IR.