GLUCOPRIVATION ATTENUATES THE HYPOPHAGIA INDUCED BY EPINEPHRINE IN MICE

It is well known that relatively high doses of epinephrine (E) injecte d intraperitoneally (IF) produce hypophagia, possibly by an action on liver metabolism. The purpose of the present experiment was to find ou t if lipoprivation with 2-mercaptoacetate (MA, 800 mu mol/kg, IF) or g lucoprivation with either 2-deoxy-D-glucose (2DG, 500 mg/kg, TP) or 2, 5-anhydro-D-mannitol (2,5-AM, 400 mg/kg, IF) were able to modify the a norectic effect of E (300 mu g/kg). At the onset of the dark period, m ice received a first injection of saline (S) or one of the metabolic b lockers mentioned above and, 30 min later, a second injection of S or E; then 30-min food intake was measured. E alone decreased feeding by 80% (p < 0.05); this effect was nearly the same when MA was previously injected. In contrast, in the presence of 2DG or 2,5-AM, E reduced fo od intake only by 22% and 24%, respectively (not significant). Attenua tion of E-induced hypophagia by these blockers suggests the participat ion of glucose utilization pathways. Because it has been shown that 2, 5-AM acts specifically on the liver, we could additionally suggest tha t E reduces feeding by an action on glucose hepatic metabolism. Copyri ght (C) 1996 Elsevier Science Inc.