The author presents a review on candidate genes of proteins involved in the metabolism of glukose, lipids and
other metabolites (glucose carriers, insulin receptors, proinsulin, glucokinase, amyline, glycogen synthase).
One of the main causes of enhanced atherogenesis in patients with type II diabetes (NIDDM) are marked genetically
conditioned deviations of the lipid, lipoprotein and apolipoprotein metabolism. In the metabolic dyshomeostasis of
multiple metabolic syndrome participate in the process of atherogenesis also: isoforms of apolipoprotein E4, isoforms
of apolipoprotein A-IV-1/1, hyperuricaemia, raised levels of the plasminogen activator inhibitor 1 (PAI-1),
hyperfibrinogenaemia, hyperhomocysteinaemia and other metabolites (cytokines, endothelin etc.). Patients with a
greated genetic sensitivity manifest diabetes sooner and more intensely and die at a younger age in particular from
cardiovascular disease, but also on account of a higher incidence of tumours diseases.
candidate genes for type II diabetes mellitus, multiple metabolic syndrome, atherogenesis, genetic
epidemiology, insulin resistance.