肥胖中的瘦素与高血压

Bravo Paco E, Morse Stephen, Borne David M, Aguilar Erwin A, Reisin Efrain

Section of Nephrology, Department of Internal Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.

Vasc Health Risk Manag. 2006;2(2):163-9. doi: 10.2147/vhrm.2006.2.2.163.

Leptin, a peptide discovered more than 10 years ago, decreases food intake and increases sympathetic nerve activity to both thermogenic and non-thermogenic tissue. Leptin was initially believed to be an anti-obesity hormone, owing to its metabolic effects. However, obese individuals, for unknown reasons, become resistant to the satiety and weight-reducing effect of the hormone, but preserve leptin-mediated sympathetic activation to non-thermogenic tissue such as kidney, heart, and adrenal glands. Leptin has been shown to influence nitric oxide production and natriuresis, and along with chronic sympathetic activation, especially to the kidney, it may lead to sodium retention, systemic vasoconstriction, and blood pressure elevation. Consequently, leptin is currently considered to play an important role in the development of hypertension in obesity.

瘦素是一种10多年前发现的肽，它能减少食物摄入量，并增加对产热和非产热组织的交感神经活动。由于其代谢作用，瘦素最初被认为是一种抗肥胖激素。然而，出于未知原因，肥胖个体对该激素的饱腹感和减重作用产生抵抗，但保留了瘦素介导的对肾脏、心脏和肾上腺等非产热组织的交感神经激活作用。研究表明，瘦素会影响一氧化氮生成和利钠作用，并且与慢性交感神经激活（尤其是对肾脏的激活）一起，可能导致钠潴留、全身血管收缩和血压升高。因此，目前认为瘦素在肥胖相关性高血压的发生发展中起重要作用。