The British Heart Foundation Centre for Cardiovascular Science, The University of Edinburgh, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK.
Curr Hypertens Rep. 2017 Nov 14;19(12):100. doi: 10.1007/s11906-017-0797-z.
The metabolic syndrome describes a clustering of risk factors-visceral obesity, dyslipidaemia, insulin resistance, and salt-sensitive hypertension-that increases mortality related to cardiovascular disease, type 2 diabetes, cancer, and non-alcoholic fatty liver disease. The prevalence of these concurrent comorbidities is ~ 25-30% worldwide, and metabolic syndrome therefore presents a significant global public health burden. Evidence from clinical and preclinical studies indicates that glucocorticoid excess is a key causal feature of metabolic syndrome. This is not increased systemic in circulating cortisol, rather increased bioavailability of active glucocorticoids within tissues. This review examines the role of covert glucocorticoid excess on the hypertension of the metabolic syndrome. Here, the role of the 11β-hydroxysteroid dehydrogenase enzymes, which exert intracrine and paracrine control over glucocorticoid signalling, is examined. 11βHSD1 amplifies glucocorticoid action in cells and contributes to hypertension through direct and indirect effects on the kidney and vasculature. The deactivation of glucocorticoid by 11βHSD2 controls ligand access to glucocorticoid and mineralocorticoid receptors: loss of function promotes salt retention and hypertension. As for hypertension in general, high blood pressure in the metabolic syndrome reflects a complex interaction between multiple systems. The clear association between high dietary salt, glucocorticoid production, and metabolic disorders has major relevance for human health and warrants systematic evaluation.
代谢综合征描述了一组风险因素的聚集，包括内脏肥胖、血脂异常、胰岛素抵抗和盐敏感型高血压，这些因素增加了与心血管疾病、2 型糖尿病、癌症和非酒精性脂肪肝疾病相关的死亡率。这些并发疾病的患病率在全球范围内约为 25-30%，因此代谢综合征对全球公共卫生构成了重大负担。临床和临床前研究的证据表明，糖皮质激素过多是代谢综合征的一个关键致病特征。这不是循环皮质醇的系统性增加，而是组织内活性糖皮质激素的生物利用度增加。这篇综述探讨了隐性糖皮质激素过多在代谢综合征高血压中的作用。在这里，检查了 11β-羟类固醇脱氢酶酶的作用，这些酶对内源和旁分泌控制糖皮质激素信号传导。11βHSD1 在细胞中放大糖皮质激素的作用，并通过对肾脏和血管的直接和间接影响导致高血压。11βHSD2 使糖皮质激素失活控制配体对糖皮质激素和盐皮质激素受体的访问：功能丧失促进盐潴留和高血压。与一般高血压一样，代谢综合征中的高血压反映了多个系统之间的复杂相互作用。高膳食盐、糖皮质激素产生和代谢紊乱之间的明显关联对人类健康具有重要意义，值得系统评估。
