Sulfonylurea drugs stimulate the 1st phase of insulin secretion, activate adenylate cyclase, inhibit phosphodiesterase or cause prolonged depolarization of the beta cell membrane. The peripheral effect of the hypoglycemic action of sulfonylurea drugs is mediated through the effect on insulin receptors. It is clearly shown that sulfonylureas lead to an increase in the number of receptors on target cells (hepatocytes, muscle and adipose tissue, lymphocytes and other cells). It is known that patients with type II diabetes mellitus have a decrease in both the number of receptors and their affinity. The increase in the number of receptors on the membrane of target cells is not due to their de novo synthesis, but by improving the return of the receptor to the membrane from the cytosol, where they are translocated as an insulin-receptor complex after the interaction of insulin with the corresponding receptor. One of the sulfonylurea drugs of the second generation is Gliquidone (glurenorm). This drug has one advantage, distinguishing it from other sulfonylurea drugs. About 95% of the drug is excreted from the body through the gastrointestinal tract, and only 5% is extracted by the kidneys. Therefore, it is the drug of choice in the treatment of diabetic patients with nephropathy, given the fact that the drug is metabolized in the liver and eliminated through the bile ducts into the intestine. Naturally, the question arises of the possibility of its influence on the liver function of patients who have been receiving long-term treatment with glurenorm.