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IH, 1Cardoso FS, 1Moura EG, 1 Lisboa PC.

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Laboratory of Endocrine Physiology, Roberto Alcantara Gomes Biology Institute and Laboratory of Molecular Endocrinology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, RJ, Brazil. Aim: Several studies reveal that nutritional, hormonal and environmental factors at prenatal and neonatal period may influence organs and tissues development, and this could be related with late diseases, like diabetes and cardiovascular disturbances (1, 2). Postnatal overfeeding increases development risk to obesity and cardiovascular diseases. It has been shown that overfed neonate rats show higher visceral adiposity and hyperleptinemia at weaning and they were programmed for obesity, higher food intake and hypertension at adulthood (3). Previously, we evidenced that neonatal hyperleptinemia induces adrenal medullary hyperfunction in early and late life (4). In the present study, we evaluated the adrenal function of obese adult rats that were overfed during lactation. We also evaluated indirectly the visceral adipocyte sensitivity to serum catecholamine, through 3-adrenergic receptor (ADRB3). Methods and results: To induce early obesity by overfeeding, the litter size was reduced from ten to three male pups at third day of lactation until weaning (small litter group, SL) while the control group stayed with ten males by litter over the lactation (normal litter group, NL). After weaning, one pup from each litter (8/group) had free access to standard diet and water until the 180 days old when they were killed and were collected samples of visceral adipose tissue (VAT), liver and the adrenal glands. Significant differences had p<0.05 or less. As expected, SL rats had hyperphagia (+18%), higher body weight (+13%) and VAT mass (SL 21.5 2.7; NL 13.6 1.0). SL group presented higher adrenal catecholamine content (SL 27.5 2.9; NL 20.4 1.9) without changes in tyrosine hydroxilase (TH) content as well as corticosterone levels. However, catecholamine in vitro secretion induced by potassium was higher in SL group (SL 4,219 1,242; NL 1,400 258). ADRB3 in VAT was unchanged. Unexpected, liver glycogen content was higher in SL group (SL 0.30 0.026; NL 0.20 0.027) even though they showed normal corticosterone and higher medullary sympathetic activity. Conclusion: The higher adrenergic catecholamine profile can help to explain the reported hypertension in this model. Paradoxically, those animals had higher liver glycogen content and VAT, which suggest a participation of other factors than adrenaline, such as a preferential use of lipids as energy source, saving glycogen. Support: CNPq, FAPERJ and CAPES. References: 1 Am J Physiol Endocrinol Metab 288, E1236E1243, 2005. 2 Ann Nutr Metab. 56(2):127, 2010. 3 Exp Clin Endocrinol. 99:154-8, 1992. 4 J Physiol. 15;580(Pt. 2):629-37, 2007.