Autoimmunization of young rabbits against endogenous glucagon fails to alter food intake or growth rates

Glucagon has been repeatedly suggested as a possible putative signal peptide for the control of satiety. This suggestion is based on the observation that fasted animals injected with glucagon will not eat. Conversely, animals given glucagon antibodies experience hyperphagia and obesity. To further investigate the possible role of glucagon in appetite control, ueaned rabbits were autoimmunized using glucagon-bovine serum albumin conjugate (G-BSA). The control animals were immunized against bovine serum albumin (BSA). During the course of the experiment, weekly blood samples were analyzed for insulin, glucagon and glucose concentrations. Weekly food consumptions and body weights were also recorded. During the last week of the experiment glucose tolerance tests were performed and liver glycogen was also measured. After the third ueek of the experiment none of the animals immunized against G-BSA had any assayable blood glucagon. However, no differences in food intake, growth rates, insulin or blood glucose (both pre- and postprandial) were evident between the two groups. Two important differences were noted. The G-BSA group had considerably more liver glycogen than the control group (5.35^ vs. 2.8?$; P < .025). Additionally, glucose tolerance curves derived from each group were significantly different. The blood glucose concentrations of the animals treated with G-BSA were significantly lower (p < .05) than the concentrations of glucose in the blood of control animals. These depressed glucose concentrations were measured throughout the entire period required to reach pre-infusion blood glucose concentrations. The data do not support the possibility that glucagon is a vital hormone in the regulation of satiety.