瘦素对醛固酮分泌的调节：在肥胖相关心血管疾病中的意义。
The regulation of aldosterone secretion by leptin: implications in obesity-related cardiovascular disease.
机构信息
Vascular Biology Center (VBC), Medical College of Georgia at Augusta University, Augusta, Georgia, USA.
出版信息
Curr Opin Nephrol Hypertens. 2018 Mar;27(2):63-69. doi: 10.1097/MNH.0000000000000384.
Abstract
PURPOSE OF REVIEW
Although it has been known for some time that increases in body mass enhance aldosterone secretion, particularly in women, the origin of this elevation in aldosterone production is not well defined. Adipocyte-derived factors have emerged as potential candidates to increase aldosterone production in obesity.
RECENT FINDINGS
Emerging evidence suggests the presence of a mechanistic link in which the adipocyte-derived hormone leptin stimulates aldosterone production in obesity, thereby creating a positive feedback loop for obesity-associated cardiovascular disease. In addition, recent reports give credence to the concept that this leptin-aldosterone stimulation pathway in obesity is an underlying mechanism for sex-discrepancies in obesity-associated cardiovascular disease.
SUMMARY
Leptin appears as a new direct regulator of adrenal aldosterone production and leptin-mediated aldosterone production is a novel candidate mechanism underlying obesity-associated hypertension, particularly in females.
摘要
目的综述
尽管人们已经知道一段时间了，体重增加会增强醛固酮的分泌，尤其是在女性中，但醛固酮产生增加的起源还没有很好地确定。脂肪细胞衍生的因子已成为增加肥胖中醛固酮产生的潜在候选因子。
最新发现
新出现的证据表明，在肥胖中，脂肪细胞衍生的激素瘦素刺激醛固酮的产生，存在着一种机制联系，从而为肥胖相关心血管疾病的发生创建了一个正反馈循环。此外，最近的报告也使人们相信，肥胖中这种瘦素-醛固酮刺激途径是肥胖相关心血管疾病中性别差异的潜在机制。
总结
瘦素似乎是肾上腺醛固酮产生的新的直接调节剂，瘦素介导的醛固酮产生是肥胖相关高血压的一个新的候选机制，尤其是在女性中。
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