title: [The paradox of insulin resistance].
abstract: Insulin resistance (IR) is a phenomenon which associates several serious "diseases of civilization" within the framework of Reaven's metabolic syndrome. In the submitted paper the authors describe the so-called "paradox of insulin resistance"--a paradoxical finding of inadequate insulin action under laboratory induced conditions while under "common" conditions the finding is reversed. Diabetes mellitus type 2 (with obesity) is characterized by excessive filling of cells by energetically rich substances. A low energy output, inadequate physical activity in these subjects leads to the development of regulatory mechanisms, which restrict further nutrient (glucose) uptake from blood into cells. During subsequent stages of the disease the excessive glucose uptake by adipose tissue cells and muscle is ensured by the high concentration gradient, hyperglycaemia and hyperinsulinaemia. Induction of "comparable" conditions in clamp studies leads to paradoxical results. During relative hypoglycaemia and hypoinsulinaemia (as compared with normal conditions) the tissues of the diabetic patient, due to regulatory mechanisms, take up a smaller amount of glucose than tissues of non-diabetic subjects (although under normal conditions the glucose uptake is higher). This phenomenon is called "Paradox of insulin resistance". In a major proportion of patients IR can be induced by mere maintenance of hyperinsulinaemia, it can be minimalized by reducing the nutrient intake and by increasing physical exertion. Differentiation of patients where IR is a secondary, regulatory phenomenon is one of the basic tasks of the physician. Only patients who suffer from primary disorders of insulin function, primary IR and true insulin deficiency should be treated by administration of hyperinsulinaemia inducing drugs. It is questionable how suitable it is to administer these drugs to patients who suffer from a life-style disorder and are threatened by complications associated with hyperinsulinism.
authors.affiliation: Internal I MN, Litomĕrice.
authors.forename: K
authors.initials: K
authors.lastname: Kubát
mesh_terms: D003920:Diabetes Mellitus / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology