Glucoprovation attenuates the hypophagia induced by epinephrine in mice

It is well known that relatively high doses of epinephrine (E) injected intraperitoneally (IP) produce hypophagia, possibly by an action on liver metabolism. The purpose of the present experiment was to find out if lipoprivation with 2-mercaptoacetate (MA, 800 μmol/kg, IP) or glucoprivation with either 2-deoxy-D-glucose (2DG, 500 mg/kg, IP) or 2,5-anhydro-D-mannitol (2,5-AM, 400 mg/kg, IP) were able to modify the anorectic effect of E (300 μg/kg). At the onset of the dark period, mice received a first injection of saline (S) or one of the metabolic blockers 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 food intake only by 22% and 24%, respectively (not significant). Attenuation of E-induced hypophagia by these blockers suggests the participation of glucose utilization pathways. Because it has been shown that 2,5-AM acts specifically on the liver, we could additionally suggest that E reduces feeding by an action on glucose hepatic metabolism.