Ludvik B
Universitätsklinik für Inner Medizin III, Wien.
Acta Med Austriaca. 1998;25(4-5):136-7.
Obesity is caused by a chronic imbalance between energy intake and energy expenditure. The increasing incidence of obesity over the last years is partly caused by the decreased physical activity following industrialization. Weight reduction can be achieved by decreasing energy intake and increasing energy expenditure. The fat loss induced by physical activity, however, is relatively small. Exercise helps to prevent the otherwise inevitable loss of muscle during caloric restriction. Due to the low success rate of conventional weight loss programs, the development of drugs to increase thermogenesis is subject to worldwide research. While in animal experiments stimulation of beta-3 adrenergic receptors leads to a significant weight loss, in humans these drugs fail to stimulate energy expenditure probably due to the lack of significant amounts of brown adipose tissue. The recently identified uncoupling proteins (UCP) 2 and 3 dissipate the protone gradient, thereby releasing stored energy as heat. These proteins might therefore act as potential targets for antiobesity drugs.
肥胖是由能量摄入与能量消耗之间的长期失衡引起的。过去几年肥胖发病率的上升部分是由于工业化后体力活动减少所致。减轻体重可以通过减少能量摄入和增加能量消耗来实现。然而，体育活动引起的脂肪减少相对较少。运动有助于防止在热量限制期间不可避免的肌肉流失。由于传统减肥计划的成功率较低，开发增加产热的药物已成为全球研究的课题。虽然在动物实验中，刺激β-3肾上腺素能受体会导致显著的体重减轻，但在人类中，这些药物可能由于缺乏大量棕色脂肪组织而无法刺激能量消耗。最近发现的解偶联蛋白（UCP）2和3消散质子梯度，从而将储存的能量以热量的形式释放出来。因此，这些蛋白质可能成为抗肥胖药物的潜在靶点。
