Impairment of glucostatic, adrenergic and serotoninergic feeding parallels the lack of glucoprivic signals in the golden hamster.

The administration of 2-deoxyglucose (2-DG) to several animal species, including humans, results in reduction of cellular glucose availability which evokes sympathoadrenal activation, hyperglycemia and stimulation of food intake. We have investigated the effects in the hamster of several drugs which are known to stimulate food intake and induce hyperglycemic response in other species. Golden hamsters pretreated with either 2-DG (0.5 g/kg IP), the alpha-2 adrenoceptor agonist UK-14304 (0.3 mg/kg IP) or the 5-HT1A selective agonist 8-OH-DPAT (0.03 mg/kg IP), have a significant hyperglycemic response, which is similar to the response in mice or rats. However, neither 2-DG, UK-14304 nor 8-OH-DPAT were capable of stimulating food intake in these hamsters. Previous studies in rats and mice demonstrated that hyperglycemic conditions result in activation of a hypothalamic anorectic recognition site, labeled with [3H]mazindol, as well as alpha-2 adrenoceptors, labeled with [3H]idazoxan. No such activation of [3H]mazindol nor [3H]idazoxan binding was observed in the hypothalamus of hamsters treated with 2-DG, despite a normal glycemic response. Thus, in this species an uncoupling between feeding responses and glucoprivic signals may represent a lack of ischymetric regulation of feeding.