Insulin resistance (IR) is related to metabolic syndrome, which is manifested by biochemical and physical disturbances that could be related to increased weight, atherogenic dyslipidemia, pro-inflammatory conditions, pro-thrombotic conditions, and hypertension. The process is complex, and the operating mechanisms are not well understood. Thus, this article aimed to determine the mechanisms of IR and its related serious health problems. It was found that subjects with impaired glucose-6-phosphate action and muscle glycogen production carry a 40% chance of developing type-2 diabetes mellitus. Further, the pro-inflammatory mediator interleukin-6 (IL-6) increases the insulin-induced glucose take-up by myocytes and decreases IR or increases insulin sensitivity in the entire body. Many reports documented an increase in IL-6 in the skeletal muscles of obese people. Cultured myocytes from obese diabetic individuals produce more monocyte chemo-attractant protein 1 and tumor necrotic factor alpha (TNF-α). TNF-α could affect mitochondrial function in myocytes and stimulate IR. The binding of insulin to the insulin receptors on endothelial cells activates the mitogen-activated protein kinase and the phosphatidylinositol 3-kinase pathways. In contrast to the first pathway, the second pathway is pro-atherogenic and is activated by IR. It was concluded that IR is associated with increased release of pro-inflammatory mediators, oxidative stress molecules, and modulation of insulin receptors in fatty tissues and endothelial cells.
Key words: Insulin resistance, diabetes mellitus, mechanisms, health hazards.
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