A maternal "junk-food" diet reduces sensitivity to the opioid antagonist naloxone in offspring postweaning
*FOODplus Research Centre, School of Agriculture, Food, and Wine, The University of Adelaide, Adelaide, South Australia, Australia The FASEB Journal
(Impact Factor: 5.04).
12/2012; 27(3). DOI: 10.1096/fj.12-217653
Perinatal exposure to a maternal "junk-food" 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.
Available from: Sarah J Spencer
- "A maternal diet that is high in fat or a maternal “junk food” diet leads to malformation of central reward pathways in the offspring. The rewarding nature of food is heightened and these offspring come to preferentially select high fat, high sucrose foods (Ong and Muhlhausler, 2011; Gugusheff et al., 2013). This diet in the mother leads to hyperinsulinaemia, insulin resistance, and increased fat deposition in the offspring (Albuquerque et al., 2006; Srinivasan et al., 2006; Ashino et al., 2012). "
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ABSTRACT: Feeding behavior is closely regulated by neuroendocrine mechanisms that can be influenced by stressful life events. However, the feeding response to stress varies among individuals with some increasing and others decreasing food intake after stress. In addition to the impact of acute lifestyle and genetic backgrounds, the early life environment can have a life-long influence on neuroendocrine mechanisms connecting stress to feeding behavior and may partially explain these opposing feeding responses to stress. In this review I will discuss the perinatal programming of adult hypothalamic stress and feeding circuitry. Specifically I will address how early life (prenatal and postnatal) nutrition, early life stress, and the early life hormonal profile can program the hypothalamic-pituitary-adrenal (HPA) axis, the endocrine arm of the body's response to stress long-term and how these changes can, in turn, influence the hypothalamic circuitry responsible for regulating feeding behavior. Thus, over- or under-feeding and/or stressful events during critical windows of early development can alter glucocorticoid (GC) regulation of the HPA axis, leading to changes in the GC influence on energy storage and changes in GC negative feedback on HPA axis-derived satiety signals such as corticotropin-releasing-hormone. Furthermore, peripheral hormones controlling satiety, such as leptin and insulin are altered by early life events, and can be influenced, in early life and adulthood, by stress. Importantly, these neuroendocrine signals act as trophic factors during development to stimulate connectivity throughout the hypothalamus. The interplay between these neuroendocrine signals, the perinatal environment, and activation of the stress circuitry in adulthood thus strongly influences feeding behavior and may explain why individuals have unique feeding responses to similar stressors.
Frontiers in Neuroscience 06/2013; 7(7):109. DOI:10.3389/fnins.2013.00109 · 3.66 Impact Factor
Available from: Zhi Yi Ong
- "The introduction of the standard chow diet at weaning was not, however, able to correct for deficits in total body weight because offspring of JF dams were lighter at birth and remained significantly shorter and lighter than control offspring at 6 weeks of age. Whilst there have been conflicting reports of the effect of maternal obesity and high-energy diets on offspring body weight, a number of previous studies, including our own, have reported lower body weights in offspring of obese/high-fat-fed mothers both at birth and in postnatal life (Rolls & Rowe 1982, Bayol et al. 2007, Bhattacharya et al. 2007, Ferezou-Viala et al. 2007, Ong & Muhlhausler 2011, Gugusheff et al. 2013). Importantly, however, the decrease in body weight occurs at the same time as percentage body fat mass is maintained (as in the present study) or increased, which suggests that the lower body weights are the result of deficits in lean body mass. "
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This study aimed to determine whether the negative effects of maternal 'junk food' feeding on food preferences and gene expression in the mesolimbic reward system could be reversed by weaning the offspring onto a low-fat diet.
Offspring of control (n = 11) and junk food-fed (JF, n = 12) dams were weaned onto a standard rodent chow until 6 weeks (juvenile) or 3 months (adult). They were then given free access to both chow and junk food for 3 weeks and food preferences determined. mRNA expression of key components of the mesolimbic reward system was determined by qRT-PCR at 6 weeks, 3 and 6 months of age.
In the juvenile group, both male and female JF offspring consumed more energy and carbohydrate during the junk food exposure at 6 weeks of age and had a higher body fat mass at 3 months (P < 0.05). Female juvenile JF offspring had higher tyrosine hydroxylase, dopamine receptors and dopamine active transporter expression in the ventral tegmental area (P < 0.05). In the adult group, there was no difference between control and JF offspring in energy and macronutrient intakes during exposure to junk food; however, female JF offspring had a higher body fat mass at 6 months (P < 0.05).
These results suggest that the effects of perinatal junk food exposure on food preferences and fat mass can be reversed by consuming a low-fat diet from weaning to adulthood in males. Females, however, retain a higher propensity for diet-induced obesity even after consuming a low-fat diet for an extended period after weaning.
Acta Physiologica 06/2013; 210(1). DOI:10.1111/apha.12132 · 4.38 Impact Factor
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ABSTRACT: Abstract A substantial body of literature has demonstrated that the nutritional environment an individual experiences before birth or in early infancy is a key determinant of their health outcomes across the life course. This concept, the developmental origins of health and disease (DOHaD) hypothesis, was initially focused on the adverse consequences of exposure to a suboptimal nutrient supply and provided evidence that maternal undernutrition, fetal growth restriction, and low birth weight were associated with heightened risk of central adiposity, insulin resistance, and cardiovascular disease. More recently, the epidemic rise in the incidence of maternal obesity has seen the attention of the DOHaD field turn toward identifying the impact on the offspring of exposure to an excess nutrient supply in early life. The association between maternal obesity and increased risk of obesity in the offspring has been documented in human populations worldwide, and animal models have provided critical insights into the biological mechanisms that drive this relationship. This review will discuss the important roles that programming of the adipocyte and programming of the central neural networks which control appetite and reward play in the early life programming of metabolic disease by maternal overnutrition. It will also highlight the important research gaps and challenges that remain to be addressed and provide a personal perspective on where the field should be heading in the coming 5-10 years.
Hormone molecular biology and clinical investigation 09/2013; 15(1):25-36. DOI:10.1515/hmbci-2013-0029
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