Adult male golden hamsters were given access to a variety of nutrient sources and were observed following the administration of regular insulin. It was hypothesized that if insulin produced hyperphagia in hamsters by the activation of a glucoprivic feeding mechanism, a selective increase in carbohydrate consumption would be observed. All animals received subcutaneous injections of 10, 30, 50 and 100 units/kg of insulin as well as a control injection of saline. Food consumption was recorded at +3, +6 and +24 hours after injections. In Experiment 1 hamsters having continuous access to Purina lab chow, fat (Crisco) and sucrose (sugar cubes) increased their total caloric consumption in response to insulin, but did not do so by selectively increasing their carbohydrate intake. In Experiment 2 hamsters maintained on Purina chow and sugar cubes consistently increased their carbohydrate intake as well as their total caloric consumption in response to insulin, but again the increase in carbohydrate intake was not selective; increased consumption of both sugar cubes and Purina chow occurred, and neither the proportion of total calories derived from carbohydrate nor the proportion of total calories derived from sugar cubes was affected by insulin administration. The results support the conclusion that insulin-induced hyperphagia in hamsters results from the activation of a non-glucoprivic feeding mechanism.