The article deals with estimating violations of carbohydrate and lipid metabolism in patients with arterial hypertension in combination with obesity. It also establishes the connection between metabolic disorders and the level of nesfatin-1. Materials and methods. The study involved 105 patients. All patients were divided into 2 groups: the 1st group consisted of patients with arterial hypertension and concomitant obesity (n=70), the 2nd group included patients with arterial hypertension and normal body weight (n=35). The control group consisted of 25 practically healthy people. Results and discussion. According to the results of the carbohydrate metabolism study, the following results were obtained. The patients with arterial hypertension and concomitant obesity, had the blood insulin level significantly higher at 18.28±0.31 μD/ml than the patients with arterial hypertension and normal body mass of 14.67±0.29 μD/ml (p<0.05). This fact confirms the presence of hyperinsulinemia in patients with concomitant obesity. Compared to patients in the control group, there was a significant increase in blood insulin level in patients with obesity and normal body mass. It was at 18.28±0.31 and 14.67±0.29 μD/ml, respectively, against 8.46±0.34 μD/ml (p<0.05). There was no statistically significant difference compared with patients of the 2nd and control groups (4.38±0.12 mmol/l against 3.96±0.16 mmol/l and 4.08±0.14 mmol/L, respectively) (p> 0.05) at the level of fasting blood glucose in patients of group 1. There was also a significant increase in the HOMA index in patients with hypertension and concomitant obesity. The patients with normal body mass had HOMA index of 6.12±0.14 and 4.39±0.12, respectively (p<0.05), and the patients in the control group – 1.87±0.11 (p<0.001). The elevated level of nesfatin-1 in patients with arterial hypertension and obesity was found to be 6.95±0.04 ng/ml, compared to people in the control group 4.61±0.07 ng/ml (p<0.001). According to the results of the correlation analysis, there was a direct correlation between the level of insulinemia and nesfatin-1 in all groups, the closest to those with arterial hypertension and concomitant obesity r=0.58 (p<0.01) compared with patients with arterial hypertension without obesity r=0.47 (p<0.01). This was confirmed by the correlation between the HOMA index and the level of nesfatin-1 in all groups, especially in the group with hypertension and obesity, r=0.39 and r=0.36 (p<0.01) respectively. According to the results of lipid profile evaluation of patients, there was no significant difference between the levels of total cholesterol – 4.61±0.13 mmol/l and 4.12±0.11 mmol/l, LDL – 2.79±0.09 mmol/l, and 2.29±0.12 mmol/l, HDL – values were 1.21±0.07 mmol/l and 1.43±0.06 mmol/l (p>0.05) in patients with hypertension with obesity and without it respectively. A significant difference was found between the values of VLDL – 0.61±0.03 mmol/L and 0.34±0.04 mmol/L (p<0.05) and the TG level was 1.33±0.10 mmol/L, and 0,86±0,04 (p<0,01) in patients with arterial hypertension and obesity and without it, respectively. In the group of patients with arterial hypertension with concomitant obesity, there was a correlation between the average intensity between the level of nesfatin-1 and the level of total cholesterol (r=0.58, p<0.01), LDL (r=0.47, p<0.01) and VLDL (r=0.41, p<0.01), as well as with the level of triglycerides (r=0.54, p<0.01), and the inverse correlation with the level HDL (r=-0.28, p<0.01). Conclusions. Taking into account the above said, we consider the lipid and carbohydrate metabolism in patients for arterial hypertension and obesity as being affected because the nesfatin-1 level rose to 6.95±0.04 ng/ml in comparison with the control group, where the value of this index was 3.10±0.04 ng/ml (p<0.001). In patients with arterial hypertension and obesity, nesfatin-1 was associated with hyperinsulinemia, a decrease in tissue sensitivity to insulin. The conducted research demonstrated a direct connection of the nesfatin-1 level with proatherogenic and inverse correlation with antiatherogenic subpopulations of blood cholesterol in patients with arterial hypertension combined with obesity.
Full text: PDF (Ukr) 197K