Insulin resistance is a pathological condition in which cells fail to respond normally to the hormone insulin available in blood in sufficient concentrations. According to present-day ideas, the resistance of peripheral tissues (muscle, adipose, hepatic) to insulin underlies a pathogenesis of type II diabetes. Biological effects of insulin may be divided into 4 groups:
VERY FAST (SECONDS): HYPERPOLARIZATION OF CELL MEMBRANES, CHANGES IN GLUCOSE AND ION TRANSPORT THROUGH MEMBRANES;
FAST (MINUTES): ACTIVATION OR INHIBITION OF ENZYMES, RESULTING IN PREVAILANCE OF ANABOLIC PROCEESS (GLYCOGENESIS, LYPOGENESIS, PROTEIN SYNTHESIS) AND INHIBITION OF CATABOLIC PROCESS;
SLOW (MINUTES TO HOURS): INCREASED ABSORPTION OF AMINOACIDS BY CELLS, SELECTIVE INDUCTION OR REPRESSION OF ENZYMATIC SYNTHESIS;
THE SLOWEST (FROM HOURS TO DAYS): CELL MITOGENESIS AND REPLICATION (DNA SYNTHESIS, GENE TRANSCRIPTION).
INSULIN RESISTANCE IS NOT ONLY THE PARAMETER WHICH CHARACTERIZES THE METABOLISM OF CARBOHYDRATES, BUT ALSO INCLUDES THE MEASUREMENT OF FAT AND PROTEIN METABOLISM, ENDOTHELIAL FUNCTIONS, GENES EXPRESSION, ETC.
THERE ARE MANY DISEASES AND CONDITIONS ACCOMPANIED BY INSULIN RESISTANCE AS FOLLOWS:
PHYSIOLOGICAL INSULIN RESISTANCE (ADOLESCENCE, PREGNANCY, HIGH-FAT DIET, NOCTURNAL SLEEP);
METABOLIC (DIABETES MELLITUS (DM) II TYPE, OBESITY, DECOMPENSATED DIABETES MELLITUS I TYPE, SIGNIFICANT NUTRITIONAL DEFICIENCY, ALCOHOL ABUSE);
ENDOCRINE (THYROTOXICOSIS, HYPOTHYREOSIS, CUSHING SYNDROME, ACROMEGALIA, PHEOCHROMOCYTOMA);
NON-ENDOCRINE (ESSENTIAL HYPERTENSION, HEPATIC CIRRHOSIS, RHEUMATOID ARTHRITIS, TRAUMA, BURNS, SEPSIS, SURGICAL INTERVENTIONS).
INSULIN RESISTANCE. ETIOLOGY.
Prereceptor. Production of incomplete insulin molecule is genetically conditioned.
Receptor. Decreased receptor quantity (target organs for insulin – liver, muscles, adipose tissue)
Postreceptor. Decreased cellular metabolic activity of insulin.
DECREASED TYROSINE KINASE ACTIVITY
DECREASED GLUCOSE TRANSPORTERS
DECREASED ACTIVITY OF PYRUVATE DEHYDROGENASE AND GLYCOGEN SYNTHASE
SYNTHES IS OF INSULIN ANTAGONISTS (ANTIBODIES TO INSULIN, CONTRINSULAR HORMONES)
