Role of fatty acid oxidation in food intake and hunger motivation in Syrian hamsters

Abstract

We examined the metabolic control of food intake in Syrian hamsters using methyl palmoxirate (MP), an inhibitor of fatty acid oxidation. If fatty acid oxidation plays a role in the control of food intake in hamsters, as it does in rats, it would be expected that hamsters predisposed toward lipid metabolism would increase food intake in response to inhibition of fatty acid oxidation. To the contrary, female hamsters fed a high-fat diet for several weeks and then treated with MP (0.25–100 mg/kg) did not increase food intake relative to vehicle-treated controls. Furthermore, MP treatment did not enhance food intake in hamsters that had been previously food deprived for 12 hr. Consistent with the inhibition of fatty acid oxidation, plasma levels of total ketone bodies and glucose in the MP-treated hamsters were significantly lower than those of the vehicle-treated controls. Thus, treatment with doses of MP which apparently inhibited fatty acid oxidation did not enhance food intake, even after manipulations which predispose the hamsters toward utilization of fat fuels. The control of food intake in Syrian hamsters is in marked contrast to that of rats and other mammals in which the consequences of glucose and fat metabolism interact to signal changes in food intake.