[PP.07.18] ASSOCIATION OF ADIPONECTIN GENE POLYMORPHISMS WITH BLOOD PRESSURE AND HYPERTENSION. (September 2016)

• Record Type: Journal Article
• Authors: Ivkovic, V.; Jelakovic, M.; Salihovic, M. Pericic; Tomas, Z.; Bozina, N.; Bozina, T.; Sertic, J.; Laganovic, M.; Pecin, I.; Fodor, L.J.; Vrkic, T. Zeljkovic; Karanovic, S.; Vrdoljak, A.; Jelakovic, B.
• Is Part Of: Journal of hypertension. Volume 34:(2016) Supplement 2
• Publication Date: 2016-09
• Subjects: Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/01.hjh.0000491769.05886.fd
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Objective: The role of adiponectin in hypertension (HT) is still a matter of debate. Obtained conflicting results could be mostly explained with diversity of subjects included in different studies. Our aim was to analyze association of adiponectin and its gene polymorphisms with blood pressure (BP) in a group of normotensive (NT) and untreated HT subjects with normal kidney function. Design and method: Analyses was conducted in 192 subjects (68 m; age 44 (IQR 31–53)). Those with diabetes, treated HT and chronic kidney disease (eGFR < 60 ml/min) were excluded. BP was measured using Omron M6 device following ESH/ESC guidelines. Adiponectin concentration was determined by ELISA. Genotyping was done using PCR-FRET. Genetic association analyses were done with Arlequin and haplotype analysis with Unphased. Results: There were no differences in plasma adiponectin values (mg/L) between HT and NT (9.75; iqr:7.44–17.88 vs.11.35;iqr:7.43–12.63;P = 0.17) and no associations with systolic or diastolic BP (P > 0.05). Ninety-three persons had genotype −11377C/C, 77 had −11377C/G and 18 −11377G/G; minor allele frequency (MAF) 30%, with no difference between NT and HT. Polymorphism −11377C > G was not associated with HT in the dominant, codominant, overdominant, recessive or additive model (all p > 0.05). Polymorphism −11391G > A (164 were dominant homozygots and 22 were heterozygots; MAF 12%, with no difference between NT and HT) also was not associated with HT (OR 2.12 [0.73–6.16]). Haplotype analysis established three haplotypes, C-G (freq. 64%), G-G (30%), C-A (6%) which showed no association with HT well. Conclusions: In our group of NT and untreated HT with normal kidney function adiponectin was not associated with BP even after adjustment for other risk factors. Even more, we did not find an association of two common adiponectin gene polymorphisms with HT. Adiponectin-BP relationship is complex and differs between specific populations. Our conclusions should not be extrapolated to subjects with other characteristics. Studies on larger number are needed.