A maternal "junk-food" diet reduces sensitivity to the opioid antagonist naloxone in offspring postweaning

Perinatal exposure to a maternal "junkfood" diet has been demonstrated to increase the preference for palatable diets in adult offspring. We aimed to determine whether this increased preference could be attributed to changes in μ-opioid receptor expression within the mesolimbic reward pathway. We report here that mRNA expression of the μ-opioid receptor in the ventral tegmental area (VTA) at weaning was 1.4-fold (males) and 1.9-fold (females) lower in offspring of junk-food (JF)-fed rat dams than in offspring of dams fed a standard rodent diet (control) (P<0.05). Administration of the opioid antagonist naloxone to offspring given a palatable diet postweaning significantly reduced fat intake in control offspring (males: 7.7±0.7 vs. 5.4±0.6 g/kg/d; females: 6.9±0.3 vs. 3.9±0.5g/kg/d; P<0.05), but not in male JF offspring (8.6±0.6 vs. 7.1±0.5g/kg/d) and was less effective at reducing fat intake in JF females (42.2±6.0 vs. 23.1±4.1% reduction, P<0.05). Similar findings were observed for total energy intake. Naloxone treatment did not affect intake of standard rodent feed in control or JF offspring. These findings suggest that exposure to a maternal junk-food diet results in early desensitization of the opioid system which may explain the increased preference for junk food in these offspring.