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原发性醛固酮增多症和原发性高血压中的代谢综合征:与脂联素基因变异的关系。

Metabolic syndrome in primary aldosteronism and essential hypertension: relationship to adiponectin gene variants.

机构信息

Division of Endocrinology, Azienda Ospedaliero-Universtaria, Ospedali Riuniti Umberto I-GM Lancisi-G Salesi, Università Politecnica delle Marche, Ancona, Italy.

出版信息

Nutr Metab Cardiovasc Dis. 2010 Feb;20(2):93-100. doi: 10.1016/j.numecd.2009.03.007. Epub 2009 May 29.

Abstract

BACKGROUND AND AIMS

Evidence shows that aldosterone excess is crucial for the development of cardiac and metabolic complications. Among the possible pathogenetic elements of the metabolic syndrome, adiponectin and its polymorphisms seem to confer a genetic risk for metabolic alterations and type 2 diabetes. Aims of the study were to investigate whether metabolic syndrome represents a common feature in patients with primary aldosteronism (PA) compared with essential hypertensives (EH) and to study the impact of two common adiponectin gene variants on the parameters of metabolic syndrome.

METHODS AND RESULTS

Metabolic syndrome was defined according to ATPIII criteria. Eighty-nine patients with PA and 164 matched EH were studied. In all patients with PA and in 135 EH two single nucleotide polymorphisms of the adiponectin gene, T45G and G276T, were detected. Patients with PA displayed a higher prevalence of metabolic syndrome compared with EH (45% vs. 30%, p<0.05). In patients with PA, genotypes 45T/G+G/G were associated with significantly lower values of waist circumference, HOMA-IR and serum aldosterone. In both PA patients and EH, the 276T/T genotype was associated with significantly worse metabolic profile and a higher risk for the metabolic syndrome (OR=1.5 for PA and OR=1.3 for EH).

CONCLUSIONS

Our data confirm a higher prevalence of metabolic syndrome among patients with PA compared with matched EH. Genetic analysis of T45G and G276T adiponectin gene polymorphisms showed that, while the genotypes 45G/G+G/T seemed to have a protective role on the metabolic complications, the genotype 276T/T defined PA and EH patients with a worse metabolic profile.

摘要

背景与目的

有证据表明,醛固酮过多对于心脏和代谢并发症的发展至关重要。在代谢综合征的可能发病因素中,脂联素及其多态性似乎为代谢改变和 2 型糖尿病的遗传风险提供了依据。本研究旨在探讨原发性醛固酮增多症(PA)患者的代谢综合征是否与原发性高血压(EH)患者具有共同特征,并研究两种常见脂联素基因变异对代谢综合征参数的影响。

方法和结果

根据 ATPIII 标准定义代谢综合征。研究了 89 例 PA 患者和 164 例匹配的 EH 患者。在所有 PA 患者和 135 例 EH 患者中,检测了脂联素基因的两个单核苷酸多态性 T45G 和 G276T。与 EH 相比,PA 患者的代谢综合征患病率更高(45% vs. 30%,p<0.05)。在 PA 患者中,45T/G+G/G 基因型与腰围、HOMA-IR 和血清醛固酮显著降低相关。在 PA 患者和 EH 患者中,276T/T 基因型与更差的代谢特征和代谢综合征的更高风险相关(PA 的 OR=1.5,EH 的 OR=1.3)。

结论

我们的数据证实,与匹配的 EH 相比,PA 患者的代谢综合征患病率更高。脂联素基因 T45G 和 G276T 多态性的遗传分析表明,基因型 45G/G+G/T 似乎对代谢并发症具有保护作用,而基因型 276T/T 则定义了代谢特征更差的 PA 和 EH 患者。

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