Immune metabolic view on insulin resistance

Czech version

Authors: Marián Mokáň; Peter Galajda
Authors‘ workplace: I. interná klinika JLF UK a UNM, Martin
Published in: Forum Diab 2021; 10(2): 136-141
Category:

Overview

Insulin resistance is defined as insufficient insulin metabolic effect in target tissues, including glucose utilisation in skeletal muscle, suppression of hepatic glucose production and suppression of lipolysis in fat tissue. Insulin resistance is one of central etiopathogenetic mechanisms of prediabetic states, including impaired fasting glucose and impaired glucose tolerance, metabolic syndrome and type 2 diabetes mellitus. Etiopathogenesis of insulin resistance in obesity implements expansion of dysfunctional adipose tissue with activation of immune system, induction of low grade inflammatory reaction and induction of insulin resistance by cytokine and lipids. Insulin resistance has primary adaptive importance in acute defense reaction against microorganism. Inflammatory induced insulin resistance in metabolic tissues is necessary for relocation of glucose to rapid proliferated immune cells utilized aerobic glycolysis such main energetic mechanism. Long-acting effect of insulin resistance due to expansion of adipose tissue in obesity is associated with metabolic syndrome, type 2 diabetes mellitus and cardiovascular diseases.

Keywords:

insulin resistance – low grade inflammatory reaction – inflammatory dysfunction of adipose tissue – inflammatory cytokines – saturated fatty acids

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