Intraventricular alloxan eliminates feeding elicited by 2-deoxyglucose.

Evidence suggests that alloxan reacts with membrane-bound glucoreceptors and that it competes with glucose molecules for these sites. We therefore administered small quantities of alloxan into the cerebrospinal fluid of rats to determine what effect this might have on their ability to react to changes of glucose concentration. Rats treated in this manner did not eat as much as controls in response to the intraperitoneal administration of 2-deoxyglucose or to a 24-hour fast, and they became hypoglycemic significantly sooner than controls when fasted. The data suggest that the function of brain glucoreceptors is to protect the body from sudden decreases of glucose and that these glucoreceptors play little if any role in the normal regulation or maintenance of feeding, body weight, or blood glucose concentrations.