Metabolic Syndrome: the Influence of Adipokines on the L-Arginine-NO Synthase-Nitric Oxide Signaling Pathway

Metabolic syndrome includes the following symptoms: obesity, hyperlipidemia, hypertension, insulin resistance, and cardiovascular disease. The purpose of this review is to elucidate role adipokines in regulation L-arginine-NO-synthas-NO signaling pathway pathogenesis metabolic syndrome. main questions raised are: how adipokine secretion changes, level their receptors regulated, which pathways are involved transmission signals when coupled L-arginine-NO-synthase-NO cascade. Adipokines peptide hormones that transmit a signal from adipose tissue targets brain, blood vessels, liver, pancreas, muscles, other tissues. Some have anti-inflammatory insulin-sensitive effects: adiponectin, omentin, adipolin, chemerin, progranulin. Others negative inflammatory effect development ofmetabolic syndrome: visfatin, vaspin, apelin. primarily regulate expression activity endothelial NO-synthase. They either activate an enzyme involving 5-AMP protein kinase or Akt kinase, increasing its synthesis NO tissues healthy patients: inhibit eNOS, leads decrease NO-synthase suppression mRNA bioavailability: apelin syndrome, dissociation dysfunction. It should be noted bioavailability formed by affected at many levels, including: ofNO-synthase protein; concentration L-arginine; cofactors reaction; detect maximum NO-synthase, dimerization required, posttranslational modifications important, particular, phosphorylation serine 1177 with participation kinases. kemerin cascade syndrom opens up certain opportunities for new approaches correction disorders observed analyzes results research searching PubMed databases, starting 2001 2020 using keywords names, more than half references last 5 years.