AJP - Regulatory, Integrative and Comparative Physiology, Vol 247, Issue 3 560-R566, Copyright © 1984 by American Physiological Society
Alpha 2-adrenoreceptor stimulation inhibits thermogenesis and food intake during glucoprivation in humans
D. A. Thompson, L. Penicaud and S. L. Welle
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.
