Alloxan-induced glucoprivic feeding deficits are blocked by D-glucose and amygdalin

Intracerebroventricular injection of alloxan, a pancreatic beta (B) cell cytotoxin, impairs glucoprivic feeding in rats. The goal of this experiment was to determine whether alloxan-induced impairment of glucoprivic feeding can be attenuated by agents which antagonize alloxan's toxicity in the B cell. Therefore, alloxan was co-administered into the fourth ventricle alone or in combination with D-glucose, L-glutamine, or amygdalin, all known antagonists of alloxan's B cell toxicity, or with L-glucose, which does not antagonize B cell toxicity. We found that alloxan produced deficits in glucoprivic feeding which were not attenuated by co-administration with L-glucose or L-glutamine. Alloxan/L-glucose treated rats ate 11% and 14% of control intake, respectively, after systemic administration of 2-deoxy-D-glucose (2DG, 250 mg/kg) and fourth ventricular 5-thioglucose (5TG, 120 micrograms/5 microliter). Alloxan/L-glutamine rats ate 20% and 22% of control intake after 2DG and 5TG, respectively. In contrast, D-glucose and amygdalin (15 mM) completely blocked alloxan-induced impairment of glucoprivic feeding and amygdalin (10 mM) exerted a partial protective effect. These behavioral results may indicate that in the brain, susceptibility to alloxan toxicity depends upon cellular characteristics shared with the B cell.