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重度肥胖患者体重减轻可改善内皮功能,而与 ADMA 降低无关。

Weight loss improves endothelial function independently of ADMA reduction in severe obesity.

机构信息

Department of Endocrinology and Clinical Chemistry, University of Heidelberg, Germany.

出版信息

Horm Metab Res. 2011 May;43(5):343-8. doi: 10.1055/s-0031-1271778. Epub 2011 Mar 1.

DOI:10.1055/s-0031-1271778
PMID:21365529
Abstract

This prospective study was performed in order to establish whether improvement of endothelial function after weight reduction can be explained by a decrease of elevated asymmetric dimethyl arginine (ADMA), an inhibitor of endogenous NO-synthase (eNOS). Therefore, 21 obese subjects (BMI: 41.1±6.4 kg/m(2)) were studied at baseline and after 12 weeks of weight reduction with a very low calorie diet. Biochemical and clinical parameters of endothelial function were assessed before and after weight loss. Biochemical parameters were determined by measurement of ADMA and soluble intercellular adhesion molecule (sICAM). Clinical parameters were assessed by pulse wave analysis (PWA). Weight intervention resulted in a 21.4±6.8 kg reduction of body weight from 119.7±12.8 kg at study start to 98.3±11.6 kg at study end (p<0.001). Accordingly, biochemical markers improved under weight reduction (ADMA from 0.47±0.07 mmol/l to 0.42±0.08 mmol/l; p=0.002; ICAM from 276±42 ng/ml to 236±29 ng/ml; p<0.001). Further, clinical parameters of functional endothelial function improved with an increase of deltaRI after salbutamol inhalation from -1% before to -9% after weight reduction (p=0.02). Interestingly, improvement of endothelial function correlated with improved HOMA index only (r=-0.60, p=0.04) but not with reduced ADMA levels, improved hypertension or reduced body weight. In conclusion, weight reduction with a very low calorie diet improves endothelial function measured by pulse wave velocity. The missing correlation with ADMA suggests possible further mechanisms underlying this observed effect, for example, improvement of insulin resistance.

摘要

这项前瞻性研究旨在确定减轻体重后内皮功能的改善是否可以用升高的不对称二甲基精氨酸(ADMA)的减少来解释,ADMA 是内源性一氧化氮合酶(eNOS)的抑制剂。因此,对 21 名肥胖受试者(BMI:41.1±6.4 kg/m²)进行了研究,他们在基线时和极低热量饮食减重 12 周后接受了研究。在减肥前后评估了内皮功能的生化和临床参数。通过测量 ADMA 和可溶性细胞间黏附分子(sICAM)来确定生化参数。通过脉搏波分析(PWA)评估临床参数。体重干预导致体重从研究开始时的 119.7±12.8kg 减少 21.4±6.8kg,至研究结束时的 98.3±11.6kg(p<0.001)。相应地,生化标志物在减重期间得到改善(ADMA 从 0.47±0.07mmol/l 降至 0.42±0.08mmol/l;p=0.002;ICAM 从 276±42ng/ml 降至 236±29ng/ml;p<0.001)。此外,功能性内皮功能的临床参数也得到改善,沙丁胺醇吸入后 deltaRI 从减重前的-1%增加至减重后的-9%(p=0.02)。有趣的是,内皮功能的改善仅与改善的 HOMA 指数相关(r=-0.60,p=0.04),而与 ADMA 水平降低、高血压改善或体重减轻无关。总之,极低热量饮食减重可改善脉搏波速度测量的内皮功能。与 ADMA 的缺失相关性表明,这种观察到的效应可能存在其他潜在机制,例如,胰岛素抵抗的改善。

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