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与胰岛素抵抗相关的基因在原发性醛固酮增多症患者中下调。

Genes implicated in insulin resistance are down-regulated in primary aldosteronism patients.

机构信息

Division of Internal Medicine and Hypertension, Department of Medicine and Experimental Oncology, University of Torino, Torino, Italy.

出版信息

Mol Cell Endocrinol. 2012 May 15;355(1):162-8. doi: 10.1016/j.mce.2012.02.007. Epub 2012 Feb 16.

Abstract

Primary aldosteronism (PA) patients display an increased incidence of insulin resistance. Herein we demonstrate the decreased gene expression of lipid metabolism genes PCK1, PLIN, ADIPOQ and PPARG in the visceral adipose tissue (VAT) of PA patients compared to age-, sex- and BMI-matched controls. In VAT, the expression of PCK1, PLIN, ADIPOQ and PPARG was inversely correlated with aldosterone levels; furthermore, PLIN and ADIPOQ gene expression was correlated with potassium levels. Therefore, raised aldosterone and low potassium may contribute to the reduced expression of these genes in PA patients. Finally, incubation of primary cultures of human adipocytes with aldosterone resulted in a decrease in the expression of PCK1, PLIN and ADIPOQ and this effect was blocked by eplerenone. Therefore, the characteristic aldosterone excess of PA patients may mediate the down-regulation of PCK1, PLIN and ADIPOQ in VAT that in turn may contribute to the insulin resistance observed in PA patients.

摘要

原发性醛固酮增多症(PA)患者表现出更高的胰岛素抵抗发生率。在此,我们证明与年龄、性别和 BMI 相匹配的对照组相比,PA 患者内脏脂肪组织(VAT)中脂质代谢基因 PCK1、PLIN、ADIPOQ 和 PPARG 的基因表达降低。在 VAT 中,PCK1、PLIN、ADIPOQ 和 PPARG 的表达与醛固酮水平呈负相关;此外,PLIN 和 ADIPOQ 基因表达与钾水平相关。因此,升高的醛固酮和低血钾可能导致这些基因在 PA 患者中的表达降低。最后,用醛固酮孵育人脂肪细胞原代培养物可导致 PCK1、PLIN 和 ADIPOQ 的表达降低,而这种作用可被依普利酮阻断。因此,PA 患者特征性的醛固酮过多可能介导 VAT 中 PCK1、PLIN 和 ADIPOQ 的下调,进而可能导致 PA 患者观察到的胰岛素抵抗。

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