ARTICLE IN PRESS 306
Abstracts / Appetite 49 (2007) 272–341
Maladaptive changes in response to a choice diet with fat and sugar S.E. LA FLEUR, A.J. VAN ROZEN, M.C.M. LUIJENDIJK,
Lj.M.J. VANDERSCHUREN, R.A.H. ADAN. Department of Pharmacology and Anatomy, Rudolf Magnus Institute of Neuroscience, Utrecht, The Netherlands The increased intake of saturated fat and sugar-based beverages has been linked to obesity. It is, therefore, important to study the regulation of consumption of dietary fat and sugar in solution and their role in the development of obesity. We subjected rats to lard and a 30% sucrose solution in addition to normal balanced chow and water (a high-fat high sucrose (HFHS)-choice diet). Rats on this HFHS-choice diet do not compensate, but increase caloric intake by 20% and rapidly develop abdominal obesity within the first two weeks. We next determined whether changes in neuropeptide expression were underlying the feeding response to a HFHS-choice diet. We subjected rats to a HFHS-choice diet or a chow diet for one week and measured neuropeptides and receptor binding in the arcuate nucleus. Interestingly, in rats on a HFHS-choice diet, we found adaptations that promote feeding: neuropeptide Y mRNA was increased, whereas proopiomelanortin mRNA and melanocortin receptor binding were decreased compared to controls. To further characterize the changes in feeding behavior, we measured the effect of a HFHS-choice diet on the motivation to work for a sucrose reward. Using a progressive ratio schedule of reinforcement, we found that consuming a HFHS-choice diet increases the motivation for sucrose. We hypothesize that changes in NPY and melanocortins underlie the effects of a HFHS-choice diet on the motivation to eat, which results in hyperphagia and obesity. This work is supported by the Netherlands Organization for Scientific Research (ZonMW/VENI).
neuropeptide system is engaged during times of negative energy balance, we hypothesized that NPY may directly modulate GRP mRNA expression in the PVN during food deprivation. To address this question we examined whether GRP-containing neurons in the PVN expressed Y1 and Y5 receptors, two NPY receptor subtypes that have been implicated in food intake and energy balance. Double label in situ hybridization was accomplished by hybridization with a combination of radiolabeled probes for either Y1 and Y5 receptors and a digoxigenin-labeled probe for GRP. Emulsion autoradiography was used to detect NPY receptors and Cy3 was used for detection of GRP. Our results indicated that both GRP mRNA and Y1 and Y5 receptor mRNA’s were co-localized in this hypothalamic region. This finding supports the possibility that the activity of GRP neurons in the PVN is directly linked to NPY signaling and may contribute to changes in GRP gene expression produced by food deprivation. Supported by NIH DK-046448. 10.1016/j.appet.2007.03.115
10.1016/j.appet.2007.03.114
Sleep–wake cycles in obese children with and without binge eating episodes Y. LATZERa,b, O. TZISCHINSKY, S. ROERa. a
Faculty of Social Welfare and Health Studies. University of Haifa Haifa, Israel bDepartment of Behavioral Studies, Emek Yezreel College, Emek Yezreel, Israel. cEating Disorders Clinic, Rambam Medical Center, Haifa, Israel
Neuropeptide Y Y1 and Y5 receptors are co-expressed with GRP mRNA in the rat hypothalamic paraventricular nucleus
E.E. LADENHEIM, R.R. BEHLES, S.BI, T.H. MORAN. Johns Hopkins University School of Medicine, Department of Psychiatry and Behavioral Sciences, Baltimore, MD, USA A number of hypothalamic neuropeptide systems have been shown to participate in energy homeostasis. We have previously reported that food deprivation time-dependently decreased gastrin-releasing peptide (GRP) gene expression in the medial parvocellular portion of the hypothalamic paraventricular nucleus (PVN) in rats. This region of the hypothalamus receives a dense projection of neuropeptide Y (NPY) neurons from the arcuate nucleus and also expresses NPY receptors. Because this
Objective: The aim of the study was to assess binge-eating episodes and to characterize sleep-wake cycles among obese children. Method: The Obese group consisted of 36 children. All participants received a diagnosis of primary obesity, with no psychiatric or organic background. The Obese group was subdivided into two groups: Obese with Binge Eating and without Binge Eating. A Normal Weight control group was comprised of 25 normal weight children. Sleep–wake patterns were monitored for 1 week, using mini-actigraphs and self-report questionnaires. Results: Thirty-seven percent of the obese children reported uncontrolled binge eating episodes. Actigraphic monitoring revealed significant differences in sleep quality between all three groups. Self-report questionnaires presented significantly more sleep disturbances in the Obese group with Binge Eating and Obese group without Binge Eating than in the Normal Weight group. Discussion: sleep disruption in Obese children with Binge Eating is significantly more severe than in both Obese non-Binge Eating children and Normal Weight controls. Correspondence Prof. Yael Latzer,
[email protected] 10.1016/j.appet.2007.03.116