Intraventricular insulin decreases kappa opioid-mediated sucrose intake in rats.

The hormone insulin acts in the central nervous system (CNS) as a regulator of body adiposity and food intake. Recent work from our laboratory has provided evidence that one way by which insulin may decrease food intake is by decreasing the rewarding properties of food. Evidence from others suggests that endogenous opioids may mediate the palatable properties of foods, and insulin may decrease nonfood-related reward via interaction with some CNS kappa opioid systems. In the present study we examined the ability of insulin to interact with exogenous or endogenous kappa opioids to modulate feeding of palatable sucrose pellets by nondeprived rats. Insulin (5 mU intracerebroventricular (i.c.v.), t=-3h) completely reversed the ability of the exogenous kappa agonist U50,488 (26 microg, i.c.v., t=-15 min) to stimulate 90-min sucrose feeding (211+/-32% reduced to 125+/-23% of 90-min baseline intake). Further, i.c.v. insulin (5 mU, t=-3h) interacted with a subthreshold dose of the kappa receptor antagonist norbinaltorphimine (5 microg, i.c.v., t=-15 min) to decrease the 90-min sucrose intake baseline (77+/-11% versus 109+/-10% of 90 min baseline intake, insulin/norbinaltorphimine versus norbinaltorphimine). Together these studies provide new evidence that insulin in the CNS may decrease the action of CNS kappa opioid system(s) that mediate palatable feeding.