Alpha 2-adrenoreceptor stimulation inhibits thermogenesis and food intake during glucoprivation in humans.

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.