Endocrine Hypertension Research Centre, The University of Queensland Diamantina Institute & Princess Alexandra Hospital, Brisbane, QLD, 4102, Australia.
Department of Endocrinology & Diabetes, Princess Alexandra Hospital, Brisbane, QLD, 4102, Australia.
J Hum Hypertens. 2021 Feb;35(2):117-123. doi: 10.1038/s41371-020-00467-3. Epub 2021 Feb 1.
Metabolic syndrome is a cluster of conditions that increase the risk of cardiovascular diseases, and comprises obesity, hypertension, impaired glucose metabolism and dyslipidaemia. It is well recognised that the mineralocorticoid receptor (MR) plays an important role in blood pressure regulation via its effect on salt and water retention in renal tubules, with hypertension being a key feature in primary aldosteronism patients with excess adrenal production of aldosterone, the primary ligand for MRs in the epithelial tissues. MRs are also expressed in a number of non-epithelial tissues including adipose tissue; in these tissues, glucocorticoids or cortisol can also activate MRs due to low levels of 11-beta-hydroxysteroid-dehydrogenase type 2 (11-βHSD2), the enzyme which inactivates cortisol. There is increasing evidence suggesting that over-activation of MRs plays a role in the pathophysiology of the other components of metabolic syndrome, promoting adiposity, inflammation and glucose intolerance, and that MR antagonists may confer beneficial effects on energy and substrate homeostasis and cardiometabolic diseases. This review discusses the advances in the literature shedding light on the MR as an emerging player in metabolic syndrome.
代谢综合征是一组会增加心血管疾病风险的病症，包括肥胖、高血压、葡萄糖代谢受损和血脂异常。众所周知，醛固酮受体（MR）通过影响肾脏小管中盐和水的保留来在血压调节中发挥重要作用，而高血压是原发性醛固酮增多症患者的一个关键特征，原发性醛固酮增多症患者的肾上腺会过量产生 MR 的主要配体醛固酮。MR 也在许多非上皮组织中表达，包括脂肪组织；在这些组织中，由于 11-β 羟类固醇脱氢酶 2（11-βHSD2）水平较低，糖皮质激素或皮质醇也可以激活 MR，11-βHSD2 是使皮质醇失活的酶。越来越多的证据表明，MR 的过度激活在代谢综合征其他成分的病理生理学中发挥作用，促进肥胖、炎症和葡萄糖不耐受，而 MR 拮抗剂可能对能量和底物稳态以及心脏代谢疾病有益。这篇综述讨论了文献中的进展，这些进展阐明了 MR 作为代谢综合征中一个新出现的参与者的作用。
