PP.28.19

Abstract

Objective: Adipose tissue is an active endocrine organ with autocrine/paracrine and endocrine metabolic functions. The aim of the study is to investigate the levels of leptin, adiponectin and lipids in patients with Essential Arterial Hypertension (EAH) and abdominal obesity (AO) depending on genes polymorphism of PPAR-γ2 (Pro12Ala) and ACE (I/D). Design and method: Study involved 110 EAH I-III stages patients with AO 1–3 grades severity: 56.4% women, 43.6% men; mean age 53.3 ± 6.05 years. Alleles of angiotensin converting enzyme – ACE (I/D) and peroxisome proliferator-activated receptor-γ2 – PPAR-γ2 (Pro12Ala) genes were studied with PCR. Overweight/AO determined according to ATP III, NCEP criteria. Control group included 50 healthy individuals. Leptin and Adiponectin plasma levels were detected by ELISA. Lipids investigated by total cholesterol (TC), triglycerides (TG), high and low density levels cholesterol (HDL, LDL). Leptin-resistance (LR) was determined by the ratio of leptin/TG (>2.7). Results analyzed according to the ESC/ESH 2013 guidelines. Results: Leptin level increased 2.48–3.35 times (61.4 ± 9.34 ng/ml, p = 0,024) in women with EAH III, AO 2–3 with decrease of adiponectin from 82.0 ± 3.05 to 73.6 ± 2.34 ng/ml, p = 0.025. Leptin in men elevated according to EAH and AO severity, remaining 2.2 times lower than in women (27.4 ± 6.54 ng/ml, p < 0.05). The levels of TC, TG, LDL and LR were 1.27–2.24 times higher in EAH II-III women than in men (p < 0.05). Atherogenic dyslipidemia type IIb (Frederickson) prevailed in 87.1% overweight and AO EAH patients, especially in ACE gene’ D-allele carriers and PPAR-γ2 Pro12-genotype. Leptin level was 1.28–3.78 times (p < = 0.048–0.008) higher in D-allele female carriers of ACE gene and in Pro12-genotype carriers of PPAR-γ2 gene (regardless of gender). DD-genotype and Pro-allele associated with 23.1–39.8% (p < 0.05) higher concentrations of LDL cholesterol, Pro12-genotype – with 23.9% (p = 0.048) higher content of TC and 2.23 times (p < 0.01) higher LR in men. Leptin synthesis and LR data increased 1.26–4.71 times (p < = 0,021–0,001) in EAH with AO DD-genotype carriers of ACE gene and Pro12- genotype of PPAR-γ2 gene. Conclusions: Hyperleptinemia, leptin-resistance, dyslipidemia in EAH and AO patients correlates with the allelic status of the ACE (I/D) and PPAR-γ2 (Pro12Ala) genes.