Straznicky Nora E, Lambert Elisabeth A, Lambert Gavin W, Masuo Kazuko, Esler Murray D, Nestel Paul J
Cardiovascular Nutrition Laboratory, Wynn Domain, Baker Heart Research Institute, P.O. Box 6492, St. Kilda Road Central, Melbourne, Victoria 8008, Australia.
J Clin Endocrinol Metab. 2005 Nov;90(11):5998-6005. doi: 10.1210/jc.2005-0961. Epub 2005 Aug 9.
Weight reduction, the first line treatment for the metabolic syndrome, improves insulin sensitivity and associated metabolic and cardiovascular abnormalities, but there is a paucity of data regarding its effect on sympathetic nervous system (SNS) activity in this clinical setting.
The objectives of this study were to test the hypothesis that dietary weight loss attenuates both insulin resistance and SNS activity and to examine the relationships between SNS activity and metabolic syndrome (MetS) components.
This was a single-sample, repeated measures design study.
This study was performed at a tertiary referral center.
Twenty-three MetS subjects (age, 58 +/- 2 yr; body mass index, 33.3 +/- 0.8 kg/m2; mean +/- sem) were studied.
A hypocaloric modified Dietary Approaches to Stop Hypertension diet (26% fat, 22% protein, and 51% carbohydrate; 100 mmol/d sodium) was consumed for 3 months.
The main outcome measures were postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve), whole-body plasma norepinephrine spillover rate, spontaneous cardiac baroreflex function, and insulin sensitivity.
The hypocaloric diet significantly reduced body weight by 7% and improved all MetS components. Norepinephrine spillover decreased from 877 +/- 180 to 503 +/- 39 ng/min (P = 0.005), and muscle sympathetic nerve activity decreased from 40.6 +/- 2.1 to 34.6 +/- 2.4 bursts/min (P = 0.01), whereas cardiac baroreflex sensitivity increased by 23.0 +/- 8.0% (P = 0.02). The change in the norepinephrine spillover rate correlated positively and independently with the change in plasma leptin concentration (r = 0.49; P = 0.03).
Weight loss by a hypocaloric diet with moderate sodium restriction diminishes SNS activity in MetS subjects. This may be due to the consequences of decreased leptin concentration, enhanced insulin sensitivity, or improvements in cardiac baroreflex function.
减重作为代谢综合征的一线治疗方法,可改善胰岛素敏感性以及相关的代谢和心血管异常,但在这种临床情况下,关于其对交感神经系统(SNS)活性影响的数据却很匮乏。
本研究的目的是检验饮食减重可减轻胰岛素抵抗和SNS活性这一假设,并研究SNS活性与代谢综合征(MetS)各组分之间的关系。
这是一项单样本重复测量设计研究。
本研究在一家三级转诊中心进行。
对23名代谢综合征受试者(年龄58±2岁;体重指数33.3±0.8kg/m²;均值±标准误)进行了研究。
采用低热量改良的终止高血压饮食法(脂肪26%、蛋白质22%、碳水化合物51%;钠100mmol/d),持续3个月。
主要观察指标为节后肌肉交感神经活性(腓总神经微神经图)、全身血浆去甲肾上腺素溢出率、自发性心脏压力反射功能和胰岛素敏感性。
低热量饮食使体重显著降低7%,并改善了所有代谢综合征组分。去甲肾上腺素溢出率从877±180降至503±39ng/min(P=0.005),肌肉交感神经活性从40.6±2.1降至34.6±2.4次/分钟(P=0.01),而心脏压力反射敏感性增加了23.0±8.0%(P=0.