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首页> 外文期刊>Nutrition, metabolism, and cardiovascular diseases: NMCD >Metabolic syndrome in primary aldosteronism and essential hypertension: relationship to adiponectin gene variants.
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Metabolic syndrome in primary aldosteronism and essential hypertension: relationship to adiponectin gene variants.

机译:原发性醛固酮增多症和原发性高血压的代谢综合征:与脂联素基因变异的关系。

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摘要

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.
机译:背景与目的:有证据表明,醛固酮过量对于心脏和代谢并发症的发生至关重要。在代谢综合征的可能的致病因素中,脂联素及其多态性似乎赋予了代谢改变和2型糖尿病的遗传风险。该研究的目的是研究与原发性高血压(EH)相比,代谢综合征是否代表原发性醛固酮增多症(PA)患者的共同特征,并研究两种常见的脂联素基因变异对代谢综合征参数的影响。方法与结果:代谢综合征是根据ATPIII标准定义的。研究了89例PA和164例匹配的EH患者。在所有患有PA和135 EH的患者中,检测到脂联素基因T45G和G276T的两个单核苷酸多态性。与EH相比,PA患者的代谢综合征患病率更高(45%比30%,p <0.05)。在PA患者中,基因型45T / G + G / G与腰围,HOMA-IR和血清醛固酮的值显着降低有关。在PA患者和EH中,276T / T基因型与代谢状况显着恶化和代谢综合征风险较高相关(PA为OR = 1.5,EH为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。 T45G和G276T脂联素基因多态性的遗传分析表明,尽管45G / G + G / T基因型对代谢并发症具有保护作用,但276T / T基因型定义了PA和EH患者的代谢状况较差。

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