Pidruchna Svitlana, Zakharchuk Uliana, Svan Olga, Zablotskyi Bohdan, Tokarskyy Oleksandr
1Ivan Horbachevsky Ternopil National Medical University, Ternopil, Ukraine.
2MSD Biotech, Swords, Dublin, Ireland.
Endocr Regul. 2025 Mar 12;59(1):17-23. doi: 10.2478/enr-2025-0003. Print 2025 Jan 1.
Genetic factors contribute to the development of metabolic syndrome and subsequent arterial hypertension (AH). The study of the T786C polymorphism of the endothelial nitric oxide synthase (eNOS) gene in arterial hypertension is important as its correlation with adipokine imbalance is a novelty area to find associations between hypertension development, obesity, and heredity. The purpose of the current study was to investigate serum adipokines levels, depending on the T786C polymorphism of the eNOS in patients with arterial hypertension. We examined 86 patients with arterial hypertension who underwent the determination of the T786C-gene promoter eNOS allelic polymorphism by PCR with electrophoretic detection. Additionally, the serum adipokines (resistin, leptin, adipoleptin, and ghrelin) levels were determined using enzyme-linked immunosorbent assay. In the patients with arterial hypertension, a significant increase in resistin level was found only in TC and CC genotype carriers of T786C, while adiponectin and leptin levels were significantly higher in all three genotypes (TT, TC, CC) compared to control healthy group. The most severe increase in the adipokine levels was observed in CC genotype, followed by TC geno-type. The antianorexic hormone ghrelin had an opposite trend, with the lowest levels found in CC, followed by TC, and TT genotypes of T786C promoter eNOS gene. Interestingly, ghrelin level in TT genotype patients was not statistically different from control healthy group. We demonstrated that CC and TC, compared with TT genotype carriers of the T786C polymorphism of the promoter eNOS gene, had significantly higher levels of all adipokines, except ghrelin, where an opposite trend was observed, which suggests their higher risk in development of more severe arterial hypertension with concomitant obesity, and other associated disorders.
遗传因素促成代谢综合征及随后的动脉高血压（AH）的发展。内皮型一氧化氮合酶（eNOS）基因T786C多态性在动脉高血压中的研究很重要，因为其与脂肪因子失衡的相关性是发现高血压发展、肥胖和遗传之间关联的一个新领域。本研究的目的是根据动脉高血压患者中eNOS的T786C多态性来研究血清脂肪因子水平。我们检查了86例动脉高血压患者，这些患者通过聚合酶链反应（PCR）及电泳检测进行了T786C基因启动子eNOS等位基因多态性的测定。此外，使用酶联免疫吸附测定法测定血清脂肪因子（抵抗素、瘦素、脂联素和胃饥饿素）水平。在动脉高血压患者中，仅在T786C的TC和CC基因型携带者中发现抵抗素水平显著升高，而与健康对照组相比，所有三种基因型（TT、TC、CC）的脂联素和瘦素水平均显著更高。在CC基因型中观察到脂肪因子水平升高最为严重，其次是TC基因型。抗厌食激素胃饥饿素呈现相反趋势，在T786C启动子eNOS基因的CC基因型中水平最低，其次是TC基因型，然后是TT基因型。有趣的是，TT基因型患者的胃饥饿素水平与健康对照组无统计学差异。我们证明，与启动子eNOS基因T786C多态性的TT基因型携带者相比，CC和TC基因型的所有脂肪因子（胃饥饿素除外）水平显著更高，而胃饥饿素呈现相反趋势，这表明它们在伴有肥胖及其他相关疾病的更严重动脉高血压发展中风险更高。
