Association of circulating adiponectin, resistin, irisin, nesfatin-1, apelin-12 and obestatin levels with hypertension and obesity

Abstract

Aim of study – examine the association between circulating blood adipokine levels (adiponectin, resistin, irisin, nesfatin-1, apelin-12 and obestatin) and hypertension and obesity. The study included a comprehensive survey of 98 patients, including 52 subjects with hypertension and 46 with hypertension and obesity. The levels of adiponectin, resistin, irisin, nesfatin-1, apelin-12, obestatin has been determined. On conducting an analysis of the study population, the circulating level of resistin (19.32±0.53 ng/mL vs. 14.90±0.29 ng/mL, p=0.0024) was higher in obese subjects with hypertension than in those without obesity, whereas apelin-12 (1.51±0.09 ng/mL vs. 1.42±0.04 ng/mL, p=0.069) and obestatin (2.97±0.04 ng/mL vs. 3.06±0.04 ng/mL, p=0.073) levels were not different between the two groups. The circulating levels of adiponectin (6.83±0.10 ng/mL vs. 2.54±0.72 ng/mL, p=0.00038), irisin (1.91±0.06 ng/mL vs. 1.19±0.03 ng/mL, p=0.021) and nesfatin-1 (8.07±0.06 ng/mL vs. 6.95±0.04 ng/mL, p=0.0057) were higher in subjects with hypertension than in those with obesity. Patients in the highest tertile of resistin were more likely to have obesity and subjects in the highest tertile of adiponectin and nesfatin-1 were more likely to have hypertension. Apelin-12 and obestatin levels in plasma did not differ according to the presence or absence of obesity. The fact that the level of resistin is highest in patients with hypertension and obesity in comparison with patients with hypertension without obesity, and the level of adipokines such as adiponectin, nesfatin-1 and irisin is higher in patients with hypertension without obesity in comparison with patients with hypertension and obesity may indicate a possible different pathogenetic role of the studied adipokines in the development of cardiovascular diseases. Since the cellular and molecular mechanisms of these changes are not definitively established and there are conflicting data in the literature, further research is needed to clarify the mechanisms of the pathogenetic role of the studied adipokines in the development of cardiovascular diseases.