title: [The role of adipokines in formation of lipid and carbohydrate metabolic disorders in patients with cardiovascular disease].
abstract: Cardio-vascular disease is an important public health problem in all developed countries.The challenge isto learn thepathogenic mechanisms of this disease.Attention of scientists of the world are drown to the role of hormones in the development of adipose tissue metabolic disorders. Adipose tissue is composed of adipocytes embedded in a loose connective tissue meshwork containing adipocyte precursors, fibroblasts, immune cells, and various other cell types. Adipose tissue was traditionally considered an energy storage depot with few interesting attributes. Due to the dramatic rise in obesity and its metabolic sequelae during the past decades, adipose tissue gained tremendous scientific interest. It is now regarded as an active endocrine organ that, in addition to regulating fat mass and nutrient homeostasis, releases a large number of bioactive mediators (adipokines) modulating hemostasis, blood pressure, lipid and glucose metabolism, inflammation, and atherosclerosis.  The aim of our study was to examine the metabolic disorders in patients with cardiovascular disease. Based on identifying the nature of changes of insulin antagonists and of insulin sensitizers. We were investigated 68 patients with hypertension, which included 35 women and 33 men.Estimated distance of carbohydrate and lipid metabolism and adipose tissue hormone imbalance.  Our results suggest that the mechanisms underlying the progression of diabetes and obesity in patients with hypertension against metabolic disorders that manifest dysfunction of carbohydrate and lipid metabolism are associated with insulinorezistense and hypervisfatinemia and hyperrezistinemia against hypoadiponektinemia occur in hypertensive patients by having diabetes mellitus type 2.
authors.affiliation: Kharkiv National Medical University, Internal Medicine Department №2, Clinical Iimmunology and Allergology, Ukraine.
authors.forename: P
authors.initials: P
authors.lastname: Kravchun
authors.forename: O
authors.initials: O
authors.lastname: Kadykova
authors.forename: T
authors.initials: T
authors.lastname: Gabisoniia
mesh_terms: D054392:Adipokines / Q000378:metabolism*; D052242:Adiponectin / Q000097:blood; D000273:Adipose Tissue / Q000378:metabolism* / Q000473:pathology; D001786:Blood Glucose / Q000378:metabolism; D050260:Carbohydrate Metabolism; D002318:Cardiovascular Diseases / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D016022:Case-Control Studies; D016207:Cytokines / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000503:physiopathology; D050171:Dyslipidemias / Q000378:metabolism / Q000503:physiopathology; D005260:Female; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008297:Male; D008659:Metabolic Diseases / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D008875:Middle Aged; D054409:Nicotinamide Phosphoribosyltransferase / Q000097:blood; D009765:Obesity / Q000209:etiology / Q000378:metabolism; D052243:Resistin / Q000097:blood
chemical_list: C499918:ADIPOQ protein, human; D054392:Adipokines; D052242:Adiponectin; D001786:Blood Glucose; D016207:Cytokines; C499624:RETN protein, human; D052243:Resistin; D054409:Nicotinamide Phosphoribosyltransferase; C085455:nicotinamide phosphoribosyltransferase, human