Adipokine levels and T786C polymorphism of eNOS gene promoter correlation in patients with arterial hypertension.

Q3 Medicine
Endocrine regulations Pub Date : 2025-03-12 Print Date: 2025-01-01 DOI:10.2478/enr-2025-0003
Svitlana Pidruchna, Uliana Zakharchuk, Olga Svan, Bohdan Zablotskyi, Oleksandr Tokarskyy
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Abstract

Objective. 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. Methods. 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. Results. 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. Conclusions. 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.

高血压患者脂肪因子水平与eNOS基因启动子T786C多态性的相关性
目标。遗传因素有助于代谢综合征和随后的动脉高血压(AH)的发展。动脉高血压患者内皮型一氧化氮合酶(eNOS)基因T786C多态性的研究具有重要意义,因为其与脂肪因子失衡的相关性是发现高血压发生、肥胖和遗传之间关系的新领域。本研究的目的是研究动脉高血压患者血清脂肪因子水平与eNOS T786C多态性的关系。方法。我们对86例高血压患者进行了t786c基因启动子eNOS等位基因多态性的PCR电泳检测。此外,采用酶联免疫吸附法测定血清脂肪因子(抵抗素、瘦素、脂增素和饥饿素)水平。结果。在动脉性高血压患者中,抵抗素水平仅在T786C基因型携带者TC和CC中显著升高,而脂联素和瘦素水平在TT、TC、CC三种基因型中均显著高于对照健康组。脂肪因子水平在CC基因型中升高最为严重,其次是TC基因型。抗厌食症激素ghrelin的变化趋势与此相反,CC中最低,其次是TC, T786C启动子eNOS基因的TT基因型。有趣的是,TT基因型患者的ghrelin水平与对照组健康组无统计学差异。结论。我们证明,与TT基因型eNOS启动子T786C多态性携带者相比,CC和TC的所有脂肪因子水平均显著升高,但胃饥饿素的趋势相反,这表明他们患更严重的动脉高血压并伴有肥胖和其他相关疾病的风险更高。
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来源期刊
Endocrine regulations
Endocrine regulations Medicine-Endocrinology, Diabetes and Metabolism
CiteScore
2.70
自引率
0.00%
发文量
33
审稿时长
8 weeks
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