After the discovery of the method of synthesis of ursodeoxycholic acid (UDCA) and the publication of evidence confirming its ability to reduce the lithogenic properties of bile, active clinical use of UDCA began around the world. This drug, in addition to the proven choleretic, cytoprotective, litholytic, anti-apoptotic effects, has a signaling activity that allows UDCA to influence metabolic syndrome components such as hyperglycemia, hypercholesterolemia.
Under the influence of UDCA, FXR is activated in the liver, which leads to an increase in the activity of glycogen synthase and decrease in the level of glycaemia. Another mechanism by which UDCA affects glycaemia is mediated by the activation of the TGR5 membrane receptor under the influence of this bile acid, as well as the release of insulin from pancreatic β-cells and decrease in postprandial glycaemia. When taking UDCA, the concentration of glycosylated hemoglobin, insulin in the blood plasma decreases the effects of insulin resistance decrease. UDCA has a beneficial effect on the vascular wall, reducing the severity of atherosclerotic lesions and normalizing the average thickness of the intima-media complex. UDCA improves lipid metabolism by regulating the activity of the AKT/ mTOR-signaling pathway, reduces the synthesis of cholesterol, and decreases the fractional rate of cholesterol synthesis and the fractional rate of triglyceride synthesis. It is proved that UDCA administration is accompanied by a drop in the level of total cholesterol and cholesterol of low-density lipoproteins. Normalization of the metabolism of glucose, triglycerides, cholesterol and the insulin-signaling pathway under the influence of bile acids is the basis for the use of UDCA for the correction of metabolic syndrome, as well as its hepatological manifestations - NAFLD.
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