Department of Internal Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO 65212, USA.
Prog Cardiovasc Dis. 2010 Mar-Apr;52(5):401-9. doi: 10.1016/j.pcad.2009.12.004.
The prevalence of diabetes, hypertension, and cardiovascular disease (CVD) and chronic kidney disease (CKD) is increasing in concert with obesity. Insulin resistance, metabolic dyslipidemia, central obesity, albuminuria. and hypertension commonly cluster to comprise the cardiometabolic syndrome (CMS). Emerging evidence supports a shift in our understanding of the crucial role of elevated serum aldosterone in promoting insulin resistance and resistant hypertension. Aldosterone enhances tissue generation of oxygen free radicals and systemic inflammation. This increase in oxidative stress and inflammation, in turn, contributes to impaired insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. In this context, recent investigation indicates that hyperaldosteronism, which is often associated with obesity, contributes to impaired pancreatic beta-cell function as well as diminished skeletal muscle insulin metabolic signaling. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated, in part, by aldosterone's nongenomic as well as genomic signaling through the mineralocorticoid receptor (MR). In the CMS, there are increased circulating levels of glucocorticoids, which can also activate MR signaling in cardiovascular, adipose, skeletal muscle, neuronal, and liver tissue. Furthermore, there is increasing evidence that fat tissue produces a lipid soluble factor that stimulates aldosterone production from the adrenal zona glomerulosa. Recently, we have learned that MR blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation as well as reduces the progression of CVD and CKD. In summary, aldosterone excess exerts detrimental metabolic effects that contribute to the development of the CMS and resistant hypertension as well as CVD and CKD.
糖尿病、高血压、心血管疾病 (CVD) 和慢性肾脏病 (CKD) 的患病率与肥胖症一起呈上升趋势。胰岛素抵抗、代谢性血脂异常、中心性肥胖、白蛋白尿和高血压通常聚集在一起构成代谢综合征 (CMS)。新出现的证据支持我们对升高的血清醛固酮在促进胰岛素抵抗和抵抗性高血压中的关键作用的理解发生转变。醛固酮增强组织中氧自由基和全身炎症的产生。这种氧化应激和炎症的增加反过来又导致胰岛素代谢信号受损、内皮介导的血管舒张功能降低以及相关的心血管和肾脏结构和功能异常。在这种情况下,最近的研究表明,常与肥胖症相关的高醛固酮血症会导致胰岛 β 细胞功能受损以及骨骼肌胰岛素代谢信号减弱。越来越多的证据表明,与胰岛素抵抗相关的心血管和肾脏异常部分是由醛固酮通过盐皮质激素受体 (MR) 的非基因组和基因组信号介导的。在 CMS 中,循环中糖皮质激素水平升高,这也可以激活心血管、脂肪、骨骼肌、神经元和肝脏组织中的 MR 信号。此外,越来越多的证据表明脂肪组织产生一种脂溶性因子,刺激肾上腺球状带产生醛固酮。最近,我们了解到 MR 阻断可改善胰腺胰岛素释放、胰岛素介导的葡萄糖利用和内皮依赖性血管舒张,并可减少 CVD 和 CKD 的进展。总之,醛固酮过多会产生有害的代谢影响,导致 CMS 和抵抗性高血压以及 CVD 和 CKD 的发展。