Immune metabolic view on metabolic syndrome components

Authors: Peter Galajda;  Marián Mokáň
Authors‘ workplace: I. interná klinika JLF UK a UNM, Martin
Published in: Forum Diab 2021; 10(3): 165-172


Metabolic syndrome is defined as cluster of independent risk factors of type 2 diabetes mellitus and cardiovascular diseases including prediabetic states associated with insulin resistance as impaired fasting glucose, impaired glucose tolerance and/or bordering increased glycosylated haemoglobin; central obesity, atherogenic dyslipidaemia with increasing of triglyceride levels and decreasing of high density lipoprotein levels and hypertension. Etiopathogenesis of metabolic syndrome 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. Etiopathogenetic mechanisms of metabolic syndrome have primary adaptive importance in acute defence reaction against microorganism. Inflammatory induced insulin resistance in metabolic tissues is necessary for relocation of glucose to rapid proliferated immune cells utilised aerobic glycolysis such main energetic mechanism. Cytokines induced dyslipidaemia (lipaemia of sepsis) has protective value against destructive effect of endotoxin. Hypertensive sodium retention phenotype is responsible for water retention required for metabolism of proliferative immune cells and compensation of fluid losses by e.g. perspiration, vomiting and diarrhoea during infections. Their long-acting effect due to expansion of adipose tissue in obesity is associated with metabolic syndrome, type 2 diabetes mellitus and cardiovascular diseases.


dyslipidaemia – hypertensive sodium retention phenotype – inflammatory dysfunction of adipose tissue – insulin resistance – low grade inflammatory reaction – metabolic syndrome


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