Thompson D A, Pénicaud L, Welle S L
Am J Physiol. 1984 Sep;247(3 Pt 2):R560-6. doi: 10.1152/ajpregu.1984.247.3.R560.
Noradrenergic central and peripheral nervous system mechanisms for the control of food intake and thermogenesis, respectively, have been described in rats and, to a lesser extent, in humans. To examine further the role of the sympathetic nervous system in energy balance modulation during glucoprivation, the alpha 2-adrenoreceptor agonist clonidine was given to subjects receiving 2-deoxy-D-glucose, a competitive inhibitor of glucose utilization, which induces sympathetic discharge, ingestive behavior, and thermogenesis by initial actions in the central nervous system. Increases in food intake and thermogenesis in association with activation of descending sympathetic outflow during 2-deoxy-D-glucose-induced glucoprivation were totally abolished by clonidine administration. Neither increases in hunger ratings after 2-deoxy-D-glucose infusions nor basal hunger and food intake after sham infusions were decreased by clonidine treatment, which nevertheless reduced thermogenesis under basal conditions. These results clearly indicate that catecholamine-mediated thermogenesis under both stimulated and basal conditions is inhibited by central or peripheral actions of clonidine, presumably at the level of alpha 2-adrenoreceptors. The reduction in food intake brought about by clonidine treatment in subjects undergoing glucoprivic stress may be the result of potentiation of satiation or reduction of hunger during a test meal rather than decreased hunger before a test meal.
去甲肾上腺素能的中枢和外周神经系统机制分别用于控制大鼠的食物摄入和产热，在人类中也有一定程度的描述。为了进一步研究交感神经系统在糖剥夺期间能量平衡调节中的作用，将α2-肾上腺素能受体激动剂可乐定给予接受2-脱氧-D-葡萄糖的受试者，2-脱氧-D-葡萄糖是一种葡萄糖利用的竞争性抑制剂，它通过中枢神经系统的初始作用诱导交感神经放电、摄食行为和产热。可乐定给药完全消除了2-脱氧-D-葡萄糖诱导的糖剥夺期间与下行交感神经流出激活相关的食物摄入和产热增加。可乐定治疗既没有降低2-脱氧-D-葡萄糖输注后饥饿评分的增加，也没有降低假输注后的基础饥饿感和食物摄入量，不过它在基础条件下降低了产热。这些结果清楚地表明，可乐定的中枢或外周作用，可能是在α2-肾上腺素能受体水平，抑制了刺激条件和基础条件下儿茶酚胺介导的产热。可乐定治疗对经历糖剥夺应激的受试者食物摄入量的减少，可能是测试餐期间饱腹感增强或饥饿感降低的结果，而不是测试餐前饥饿感的降低。
