CAFETERIA DIET ALTERS THE EXPRESSION OF KEY GENES OF THE BRAIN REWARD SYSTEM OVER TIME

RAMOS, JORGE G; STOKER, CORA; ACUTAIN, M. FLORENCIA; ANDREOLI, M. FLORENCIA; RAMOS, JORGE G; SCHUMACHER, ROCIO; STOKER, CORA; ACUTAIN, M. FLORENCIA; LAZZARINO, GISELA PAOLA; ANDREOLI, M. FLORENCIA; SCHUMACHER, ROCIO; LAZZARINO, GISELA PAOLA

CABA

Congreso; Reunion Conjunta de Sociedades de Biociencia; 2017

SAIC

We aim to determine the effects of Cafeteria diet (CAF), rich in palatableand energy dense foods, on the expression of key genes of the brain reward system (RW) in the shortand long term. Female Wistar rats were fed chow or CAF for 4 or 11 weeks.Animals were sacrificed and 2 regions of the Accumbens Nucleus (NA ? Core, NAC; andshell, NAS), Ventral Pallidum (VP) and Ventral Tegmental Area (VTA) weredissected. Serumleptin was assessed by RIA. mRNAexpression of genes of the dopaminergic and GABAergic pathway, and the leptinreceptor (ObRb) was evaluated by qPCR in the nuclei. Datawas statistically analyzed by two-way ANOVA followed by Tukey post-test.Four weeks of CAF increased energy intake and adiposity,not affecting circulating leptin or body weight. In VTA, 4 weeks of CAF increasedthe expression of the dopamine active transporter (DAT) and decreased bothisoforms of the enzyme involved in the synthesis of GABA (glutamatedecarboxylase, GAD 1 and 2), without altering tyrosine hydroxylase (TH)expression. CAF decreased dopamine receptor (DR) 2 expression in NAS andincreased DR1 levels in NAC. Also, CAF increased GAD2 levels in VP. After 11weeks of CAF, animals sustained the hyperenergetic intake and further increasedadiposity, leading to hyperleptinemia and higher body weight, only concomitant toan increased expression of ObRb in VTA. Our results indicate that the higher energyintake of CAF animals in the short-term would respond to hedonic mechanisms,given by molecular deregulations in the RW. The palatability of the diet couldlead to a hypodopaminergic state, as DAT expression increase in VTA and DR2decrease in NAS. Besides, the increment in GAD2 expression in VP indicates an inhibitoryGABAergic input to dopaminergic and GABAergic VTA neurons that may, inhibitdopamine and GABA release, in line with the low expression levels of GAD1 andGAD2. Conversely, in the long-term the hypercaloric intake could respond to analtered homeostatic control.