Young J B, Macdonald I A
Department of Medicine, Northwestern University Medical School, Chicago, IL 60611-3008.
Int J Obes Relat Metab Disord. 1992 Dec;16(12):959-67.
Alterations in sympathetic nervous system (SNS) activity are widely believed to contribute to the pathophysiology of the obese state. Disagreement, however, exists as to whether the predominant sympathetic abnormality is a decrease in neuronal activity (leading to diminished sympathetically-mediated energy expenditure and weight gain) or an increase (leading to hypertension). Findings summarized from over 40 separate studies support both hypotheses as well as the alternative thesis that SNS activity does not differ in obese humans compared to lean controls. Another abnormality being noted with increasing frequency in human obesity is reduced adrenaline (Ad) levels in plasma, both at rest or in response to a stimulus such as physical activity. Whether diminished adrenal medullary function is a cause or consequence of the obese state and whether the adrenal medulla plays any role in the regulation of energy metabolism on a daily basis are not known at the present time. Thus, while depressed SNS activity may be a sufficient explanation for the development of obesity, it is not a necessary condition. Suppressed adrenal medullary function may also contribute to this disorder.
人们普遍认为，交感神经系统（SNS）活动的改变会导致肥胖状态的病理生理过程。然而，对于主要的交感神经异常是神经元活动减少（导致交感神经介导的能量消耗减少和体重增加）还是增加（导致高血压），存在不同观点。40多项独立研究总结的结果支持了这两种假设，以及另一种观点，即肥胖人群的SNS活动与瘦人对照组没有差异。在人类肥胖中，另一个越来越频繁被注意到的异常是血浆中肾上腺素（Ad）水平降低，无论是在静息状态还是对诸如体育活动等刺激的反应中。目前尚不清楚肾上腺髓质功能减退是肥胖状态的原因还是结果，以及肾上腺髓质在日常能量代谢调节中是否发挥任何作用。因此，虽然交感神经系统活动降低可能足以解释肥胖的发生，但这不是必要条件。肾上腺髓质功能受抑制也可能导致这种疾病。
