Landsberg L, Young J B
Department of Medicine, Northwestern University Medical School.
Int J Obes Relat Metab Disord. 1993 Feb;17 Suppl 1:S29-34.
The sympathetic nervous system is a major regulator of dietary thermogenesis in laboratory animals and humans. Since a lowered metabolic rate predisposes to the development of obesity, and since caloric restriction suppresses sympathetic activity, a role for adrenergic agonists in the treatment of obesity has a well established physiological rationale. Although diminished sympathetic activity does not appear to underlie obesity in most circumstances in humans, to the extent that adrenergic agonists increase metabolic rate in the obese they may be useful as pharmacologic adjuncts to low energy diets. During caloric restriction the significant diminution in sympathetically mediated thermogenesis antagonizes weight loss; this decrease in metabolic rate may be overcome by sympathomimetic amines thereby increasing the effectiveness of low energy diets. Since smoking stimulates the sympathoadrenal system and increases thermogenesis, smoking cessation, with its attendant fall in sympathoadrenal activity and decrease in metabolic rate, fosters weight gain. Adrenergic agonists may be useful in this circumstance as well.
交感神经系统是实验动物和人类饮食产热的主要调节者。由于代谢率降低易导致肥胖的发生，且热量限制会抑制交感神经活动，因此肾上腺素能激动剂在肥胖治疗中的作用具有充分确立的生理学依据。尽管在大多数情况下，交感神经活动减弱似乎并非人类肥胖的基础，但就肾上腺素能激动剂可提高肥胖者的代谢率而言，它们可能作为低能量饮食的药物辅助手段而有用。在热量限制期间，交感神经介导的产热显著减少会对抗体重减轻；拟交感胺类药物可克服这种代谢率的降低，从而提高低能量饮食的效果。由于吸烟会刺激交感肾上腺系统并增加产热，戒烟伴随着交感肾上腺活动的下降和代谢率的降低，会促进体重增加。在这种情况下，肾上腺素能激动剂可能也有用。
