ABSTRACT
PPARs play the key role in energy homeostasis, inflammation, development of insulin resistance, metabolic syndrome, therefore the special attention is spared to synthesis of the ligand PPARs (fibrates, thiazolidinediones). Three isoforms of PPARs are activated by the fatty acids and their derivatives - eukosanoides. Polymorphism of the Pro 12Ala gene PPARG2 affects the sensitiveness of tissues to insulin and the risk of the development diabetes. It is assumed that the PPAR polymorphism is related to the differential answer on pharmacotherapy that is the foundation for development of the personification of the drug application and the estimate of prognosis.
Subject(s)
Diabetes Mellitus/metabolism , Insulin Resistance/physiology , Peroxisome Proliferator-Activated Receptors/physiology , Animals , Cardiovascular Diseases/genetics , Cardiovascular Diseases/metabolism , Diabetes Mellitus/genetics , Dyslipidemias/genetics , Dyslipidemias/metabolism , Energy Metabolism , Humans , Insulin Resistance/genetics , Lipoproteins/metabolism , Peroxisome Proliferator-Activated Receptors/agonists , Peroxisome Proliferator-Activated Receptors/genetics , Polymorphism, Genetic , Protein IsoformsABSTRACT
Nitric oxide (NO) is synthesized from 1-arginine by endothelial nitric oxide synthase (eNOS). NO participates in regulation of physiologically important cardiovascular functions (contractive reduction of heart, cellular proliferation, a tone of vessels and blood pressure), immunity, and nervous systems. Inflammation factors, hypoxia, lipids affect NO synthesis. Intensity of eNOS gene transcription depends on polymorphic alleles of eNOS gene, posttranscriptional mechanisms providing mRNA stability. All these factors have effects on development of cardiovascular events.
Subject(s)
Cardiovascular Diseases , Endothelium, Vascular/enzymology , Gene Expression Regulation, Enzymologic , Nitric Oxide Synthase/genetics , Nitric Oxide , Animals , Cardiovascular Diseases/enzymology , Cardiovascular Diseases/etiology , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/prevention & control , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Nitric Oxide/biosynthesis , Nitric Oxide/physiology , Nitric Oxide Synthase/biosynthesis , RNA, Messenger/biosynthesis , RNA, Messenger/geneticsABSTRACT
Certain hypothermia action mechanisms on Ca2(+)-pump of the sarcoplasmic reticulum in rat myocardium autolysis are investigated. The complex dependence of Ca2(+)-transporting system preservation in autolysis on the depth of hypothermia is shown. The role of lipid peroxidation and endoproteolysis in a decrease of the autolysing myocardium Ca2(+)-pump activity is considered. A conclusion is drawn that hypothermia does not affect the accumulation of peroxidation products in sarcoplasmic reticulum membranes during myocardium autolysis. The protective action of deep hypothermia on the autolysing myocardium Ca2(+)-pump is realized, at least partially, due to an increase in the Ca2(+)-ATPase active molecules number.
