Beilerli Aferin, Kudriashov Valentin, Sufianov Albert, Kostin Andrey, Begliarzade Sema, Ilyasova Tatiana, Liang Yanchao, Mukhamedzyanov Albert, Beylerli Ozal
Department of Obstetrics and Gynecology, Tyumen State Medical University, 54 Odesskaya Street, 625023, Tyumen, Russia.
Gastric Cancer Center, West China Hospital of Sichuan University, China.
Noncoding RNA Res. 2023 Feb 16;8(2):218-223. doi: 10.1016/j.ncrna.2023.02.005. eCollection 2023 Jun.
The term "insulin resistance" is commonly understood as a decrease in the response of insulin-sensitive tissues to insulin at its sufficient concentration, leading to chronic compensatory hyperinsulinemia. Type 2 diabetes mellitus is based on mechanisms consisting in the development of resistance to insulin in target cells (hepatocytes, adipocytes, skeletal muscle cells), resulting in the termination of an adequate response of these tissues to interaction with insulin. Since in healthy people 75-80% of glucose is utilized by skeletal muscle, it is more likely that the main cause of insulin resistance is impaired insulin-stimulated glucose utilization by skeletal muscle. With insulin resistance, skeletal muscles do not respond to insulin at its normal concentration, thereby determining an increase in glucose levels and a compensatory increase in insulin production in response to this. Despite many years of studying diabetes mellitus (DM) and insulin resistance, the molecular genetic basis for the development of these pathological conditions is still the subject of numerous studies. Recent studies point to the involvement of microRNAs (miRNAs) as dynamic modifiers in the pathogenesis of various diseases. MiRNAs are a separate class of RNA molecules that play a key role in the post-transcriptional regulation of gene expression. Recent studies have shown that miRNAs dysregulation in DM is closely related to miRNAs regulatory abilities in skeletal muscle insulin resistance. This gave grounds to consider an increase or decrease in the expression of individual microRNAs in muscle tissue and consider them as new biomarkers for diagnosing and monitoring insulin resistance and promising directions for targeted therapy. This review presents the results of scientific studies examining the role of miRNAs in skeletal muscle insulin resistance.
“胰岛素抵抗”一词通常被理解为在胰岛素浓度充足时，胰岛素敏感组织对胰岛素的反应降低，从而导致慢性代偿性高胰岛素血症。2型糖尿病基于靶细胞（肝细胞、脂肪细胞、骨骼肌细胞）中胰岛素抵抗的发展机制，导致这些组织与胰岛素相互作用时无法产生足够的反应。由于在健康人群中，75%至80%的葡萄糖由骨骼肌利用，因此胰岛素抵抗的主要原因更可能是骨骼肌对胰岛素刺激的葡萄糖利用受损。出现胰岛素抵抗时，骨骼肌对正常浓度的胰岛素无反应，从而导致血糖水平升高，并促使胰岛素分泌代偿性增加。尽管对糖尿病（DM）和胰岛素抵抗进行了多年研究，但这些病理状况发生发展的分子遗传学基础仍是众多研究的课题。最近的研究指出，微小RNA（miRNA）作为动态调节因子参与了各种疾病的发病机制。miRNA是一类独特的RNA分子，在基因表达的转录后调控中起关键作用。最近的研究表明，糖尿病中miRNA失调与骨骼肌胰岛素抵抗中miRNA的调节能力密切相关。这使得人们有理由考虑肌肉组织中单个微小RNA表达的增加或减少，并将它们视为诊断和监测胰岛素抵抗的新生物标志物以及靶向治疗的潜在方向。本综述介绍了研究miRNA在骨骼肌胰岛素抵抗中作用的科学研究结果。
