Svitlana Pidruchna, Uliana Zakharchuk, Olga Svan, Bohdan Zablotskyi, Oleksandr Tokarskyy
{"title":"Adipokine levels and T786C polymorphism of eNOS gene promoter correlation in patients with arterial hypertension.","authors":"Svitlana Pidruchna, Uliana Zakharchuk, Olga Svan, Bohdan Zablotskyi, Oleksandr Tokarskyy","doi":"10.2478/enr-2025-0003","DOIUrl":null,"url":null,"abstract":"<p><p><b>Objective.</b> 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. <b>Methods.</b> 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. <b>Results.</b> 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. <b>Conclusions.</b> 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.</p>","PeriodicalId":11650,"journal":{"name":"Endocrine regulations","volume":"59 1","pages":"17-23"},"PeriodicalIF":0.0000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Endocrine regulations","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2478/enr-2025-0003","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"Print","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
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.