Abstract
The composition of leukocytes includes monocytes/macrophages and lymphocytes - cells, inflammation and infiltration of which is an important event in the pathogenesis of diabetes and related complications. The enzyme immunoassay method determined in leukocytes the level of threonine 172 phosphorylation (activation) of 5’adenosine monophosphate-activated protein kinase (AMPK), which controls the cell energy balance, in the combined treatment of patients with with insulin, metformin, gliklazidy MR and g, and the rats of heart and glyclaside MR and chromploidine, and ga; The level of threonine 172 phosphorylation (activation) of 5'-adenosine monophosphate-activated protein kinase (AMPK), controlling the energy balance of the cell, at combination treatment of patients with type 2 diabetes (T2D) with insulin, metformin, gliclazide and dapagliflozin was determined in blood cells by enzyme immunoassay. It has been shown that metformin drugs increase the activity of AMPK in the blood cells of patients with T2D more than 3-6 times compared with patients before treatment. Insulin and its analogue completely suppress AMPK activity, induced by metformin in the leucocytes of patients with T2D, which may indicate a decrease in the therapeutic effect of metformin. Gliclazide MR increases the activity of AMPK in blood mononuclear cells. In the presence of both metformin and gliclazide, the level of AMPK phosphorylation is reduced. The mechanism of activation of AMPK by gliclazide probably related to the effect of the latter on Ерас2А. Dapagliflozin increases the activity of AMPK and enhances the effect of metformin in the leucocytes of patients with T2D. AMPK activity in blood cells can serve as one of the indicators of the effectiveness of the hypoglycemic drugs action. The mechanisms of drug interaction and the consequences of their antagonism are discussed.
Highlights
By direct phosphorylation of metabolic enzymes and transcription factors, AMPK stimulates catabolic processes — absorption of glucose, fatty acids and their conversion by mitochondrial oxidation and glycolysis
The patients were divided into groups: the control group consisted of healthy individuals who did not have DM, representative by age (n = 3); patients with type 1 diabetes (T1D) on insulin therapy (n = 7); patients with type 2 diabetes before the hypoglycemic therapy (n = 2); patients with T2D receiving metformin at a dose of 1000 mg twice a day as an hypogly
Metformin increases more than three-fold the activity of AMPK in blood cells of patients with T2D, which may indicate that the drug affects muscles, liver and adipose tissue, and blood cells
Summary
By direct phosphorylation of metabolic enzymes and transcription factors, AMPK stimulates catabolic processes — absorption of glucose, fatty acids and their conversion by mitochondrial oxidation and glycolysis. At the same time, combined therapy of the first-line hypoglycemic drug metformin with insulin can lead to negative consequences and even increase the death rate of patients [7,8,9]. These facts require further study to understand the risks associated with the use of insulin and metformin in patients with diabetes. The aim of our work was the study of the activity of the main energy sensor of cells — AMPK in leucocytes from patients taking hypoglycemic drug both as monotherapy, and in combination
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