FP30-5 Perinatal High-Fat Diet Consumption Programs the Melanocortin System of Juvenile Japanese Macaques

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: FP30-Central Regulation of Appetite & Feeding
Basic
Monday, June 17, 2013: 10:45 AM-11:15 AM
Presentation Start Time: 11:05 AM
Room 304 (Moscone Center)

Poster Board MON-654
Juliana Gastao Franco*, Elinor Louise Sullivan, Elizabeth K Nousen, Diana Lynn Takahashi, Melissa Ann Kirigiti and Kevin L Grove
Oregon Health and Science University/ONPRC, Beaverton, OR
Using a nonhuman primate model, our group demonstrated that high-fat diet (HFD) consumption during gestation alters fetal development of neurons that control food intake, resulting in increased proopiomelanocortin mRNA expression and decreased agouti-related protein mRNA and protein levels. Programming of the systems that regulate energy homeostasis has been suggested as an important contributing factor for the world-wide increased prevalence of obesity in the past decades. In this study, we hypothesized that exposure to maternal HFD consumption impacts brain development of key pathways that regulate feeding and increase the risk of offspring developing obesity. Our goal was to examine how perinatal HFD consumption can cause permanent programming of the central melanocortin system, food intake, and body weight in juvenile offspring. Offspring naturally born from female Japanese macaques who consumed either a control (CTR) diet (14% fat calories) or a HFD (35% fat calories) were studied. After weaning, the offspring were either maintained on the same diet (CTR/CTR, HFD/HFD) or underwent a diet switch (CTR/HFD, HFD/CTR). Between the ages of 6-11 months of age we measured total food intake, preference of diets with different contents of fat and sugar, body composition, metabolic rate and activity. Immunohistochemistry and in situ hybridization were utilized to examine the melanocortin system in the hypothalamus. The main findings of this study indicate that maternal HFD consumption contributes to increased body weight in male offspring, with no changes in basal and total metabolic rate. Interesting, specifically HFD that were switch to a CTR diet after weaning displayed increased overall food intake and binge eating of diets with high sugar and fat. These animals also displayed an increase in the ratio of AgRP to alpha-melanocyte-stimulating hormone (α-MSH) peptide levels in paraventricular nucleus. Our results suggest that exposure to perinatal HFD can cause a permanent neurochemical change of the melanocortin system in the hypothalamus that consequently predispose offspring to an orexigenic drive for palatable and calorically dense foods, ultimately leading to increased adiposity.

Nothing to Disclose: JGF, ELS, EKN, DLT, MAK, KLG

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