Peterson H R, Rothschild M, Weinberg C R, Fell R D, McLeish K R, Pfeifer M A
Department of Medicine, School of Medicine, University of Louisville, Ky 40292.
N Engl J Med. 1988 Apr 28;318(17):1077-83. doi: 10.1056/NEJM198804283181701.
The cause of most cases of human obesity is unknown. Specific alterations in the activity of the autonomic nervous system may mediate and perhaps cause obesity in animal models. We therefore looked for alterations in autonomic activity in human obesity. Fifty-six healthy men with various percentages of body fat underwent autonomic testing while at rest. Significant correlations were found between the percentage of body fat and the variation in the R-R interval after beta-adrenergic blockade (r = -0.30, P less than 0.03), the heart rate (r = 0.30, P less than 0.03), the plasma norepinephrine concentration (r = -0.30, P less than 0.05), the plasma epinephrine concentration (r = -0.49, P less than 0.001), and the pupillary latency period (r = 0.39, P less than 0.01). Each of these variables reflects the activity of the sympathetic nervous system or parasympathetic nervous system or both. Depressions in sympathetic and parasympathetic activity were significantly but weakly associated with increasing percentages of body fat. These associations indicate that in obese persons, autonomic changes, though not necessarily causal, involve several organ systems. We suggest that autonomic alterations are important in human obesity, as they are in animal obesity. A disordered homeostatic mechanism may promote excessive storage of energy by decreasing sympathetic activity, while defending against weight gain by decreasing parasympathetic activity. The use of autonomic profiles holds promise for classifying human obesity and identifying obese patients at increased risk for various disorders.
大多数人类肥胖病例的病因尚不清楚。自主神经系统活动的特定改变可能在动物模型中介导甚至导致肥胖。因此，我们研究了人类肥胖中自主神经活动的变化。56名身体脂肪比例各异的健康男性在静息状态下接受了自主神经测试。结果发现，体脂百分比与β-肾上腺素能阻滞剂作用后R-R间期的变化（r = -0.30，P<0.03）、心率（r = 0.30，P<0.03）、血浆去甲肾上腺素浓度（r = -0.30，P<0.05）、血浆肾上腺素浓度（r = -0.49，P<0.001）以及瞳孔潜伏期（r = 0.39，P<0.01）之间存在显著相关性。这些变量中的每一个都反映了交感神经系统或副交感神经系统或两者的活动。交感神经和副交感神经活动的降低与体脂百分比的增加显著但微弱相关。这些关联表明，在肥胖者中，自主神经变化虽然不一定是因果关系，但涉及多个器官系统。我们认为，自主神经改变在人类肥胖中很重要，就像在动物肥胖中一样。一种紊乱的稳态机制可能通过降低交感神经活动来促进能量的过度储存，同时通过降低副交感神经活动来防止体重增加。利用自主神经特征有望对人类肥胖进行分类，并识别出患各种疾病风险增加的肥胖患者。
