Abstract
Abstract. In recent years, the attention of scientists has been drawn to the potential involvement of adipose tissue, particularly markers of its hormonal activity (leptin, adiponectin, tumor necrosis factor-alpha (TNF-α), and insulin β2-receptors), in the pathogenetic mechanisms of metabolic syndrome (MS).
Purpose: to evaluate the activity of proinflammatory cytokine TNF-α, levels of insulin β2-receptors, leptin and adiponectin in patients with nonalcoholic fatty liver disease (NAFLD) with MS depending on the type of insulinemia and the degree of obesity.
Material and methods. Were examined 139 patients with NAFLD and with MS. Depending on the fasting endogenous insulin (EI) level in the blood of the patients is divided into two groups: group 1 – 59 patients with normal levels of EI in the blood (34 patients with normal body weight and 25 patients with obesity); group 2 – 80 patients with spontaneous hyperinsulinemia (HI) (32 patients with normal body weight and 48 patients with obesity). Control group – 20 healthy people.
Results and Discussion. A significant increase in the level of β2-insulin receptors was observed in all examined patients. In patients with spontaneous HI and obesity, the level of β2-insulin receptors was 4.7 times higher than in healthy subjects (p<0.05) and 1.5 times higher than in patients with obesity and normal EI (p2<0.05). Hyperleptinemia and hypoadiponectinemia were observed in all patients with NAFLD and MS. In obese patients from both groups, leptin levels were were 3.7 and 5.6 times higher, respectively, compared to healthy controls (p<0.05). In patients with spontaneous hyperinsulinemia and obesity, leptin levels were 1.5 times higher than in those with normal blood EI and obesity (p1<0.05). Hypoadiponectinemia was present in all patients. Specifically, in obese patients from groups 1 and 2, adiponectin levels were decreased by 7.0% and 47.0%, respectively, compared to healthy controls (p<0.05). In patients from group 2 with obesity, adiponectin
levels were 43% lower than in those from group 1 (p2<0.05).
The level of TNF-α was significantly elevated in patients from both groups. In obese patients from groups 1 and 2, this marker was 12% and 37% higher than in the control group, respectively (p<0.05). Furthermore, in obese patients from group 2, TNF-α levels were 22% higher than in group 1 (p2<0.05).
Conclusions. Insulin hypersecretion (IH), insulin resistance (IR), hyperleptinemia, and hypoadiponectinemia play a significant role in the development and progression of nonalcoholic fatty liver disease (NAFLD) in patients with metabolic syndrome (MS). The increase in TNF-α levels in the blood leads to the activation of the cytokine cascade of the inflammatory response and exacerbates the severity of IR in patients with NAFLD and MS.
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