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人体交感神经系统活动与进食的热效应

Sympathetic nervous system activity and the thermic effect of feeding in man.

作者信息

Schwartz R S, Jaeger L F, Silberstein S, Veith R C

出版信息

Int J Obes. 1987;11(2):141-9.

PMID:3610467
Abstract

Animal studies have demonstrated an important role for the sympathetic nervous system in food-induced increases in energy expenditure. Despite studies in man showing a rise in plasma norepinephrine after a meal, no relationship has previously been demonstrated between the increment in plasma norepinephrine and the increase in energy expenditure. Because changes in plasma norepinephrine may not always accurately reflect alterations in sympathetic nervous system activity, we investigated the effects of an 800-kcal high-carbohydrate meal on both plasma norepinephrine kinetics and energy expenditure as well as their relationship to each other. A post-cibum increase in both energy expenditure (0.18 +/- 0.09 kcal/min, P less than 0.001) and plasma norepinephrine concentration (44 +/- 39 pg/ml, P less than 0.05) was noted but again no relationship between the two parameters was found. In contrast, the increment in norepinephrine appearance rate after the meal (0.11 +/- 0.09 microgram/min, P less than 0.001) was significantly correlated to the increment in energy expenditure (r = 0.57, n = 20, P less than 0.01). No change was noted in norepinephrine clearance rate after the meal. It is concluded that sympathetic nervous system induced increases in energy expenditure may account for at least part of the thermogenesis that occurs after a high-carbohydrate meal. It is postulated that individual variability in this sympathetic nervous system induced component of the thermic effect of feeding may account for some of the differences in energy expenditure noted between obese or elderly subjects and normal weight young controls after a meal.

摘要

动物研究已证明交感神经系统在食物诱导的能量消耗增加中起重要作用。尽管对人类的研究表明餐后血浆去甲肾上腺素会升高,但此前血浆去甲肾上腺素的增加与能量消耗的增加之间并未显示出相关性。由于血浆去甲肾上腺素的变化可能并不总是准确反映交感神经系统活动的改变,我们研究了一顿800千卡高碳水化合物餐对血浆去甲肾上腺素动力学和能量消耗的影响以及它们之间的相互关系。进食后能量消耗(0.18±0.09千卡/分钟,P<0.001)和血浆去甲肾上腺素浓度(44±39皮克/毫升,P<0.05)均出现餐后升高,但再次发现这两个参数之间没有关系。相反,餐后去甲肾上腺素出现率的增加(0.11±0.09微克/分钟,P<0.001)与能量消耗的增加显著相关(r=0.57,n=20,P<0.01)。餐后去甲肾上腺素清除率未发现变化。结论是交感神经系统诱导的能量消耗增加可能至少部分解释了高碳水化合物餐后发生的产热现象。据推测,进食热效应中这种交感神经系统诱导成分的个体差异可能解释了肥胖或老年受试者与正常体重年轻对照组餐后能量消耗差异的部分原因。

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