Obesity is America’s fastest growing health threat. Although a primary health risk factor, obesity increases the probability of secondary health consequences such as stroke, diabetes mellitus and heart disease. Siberian hamsters offer a convenient model to study obesity, as they exhibit a photoperiod-driven reversal of obesity during the fall-winter months (i.e., short-days-SD). SD responses in the Siberian hamster, amongst others, include decreased adiposity and gonadal regression. The duration of the dark period is faithfully transmitted into a neuroendocrine melatonin (MEL) signal; that codes seasonal information. The brain communicates with body fat (white adipose tissue- WAT) via the sympathetic nervous system (SNS). The central MEL binding sites, however, necessary for the body fat/lipid mobilization responses during SDs are not precisely known, although melatonin receptor (MEL 1aR) mRNA has been co-localized with sympathetic outflow neurons of WAT in several forebrain areas. This dissertation aims to identify and to characterize the contribution of central sites that are important in seasonal responses in Siberian hamsters. Thus, I asked: Which specific brain sites are both sufficient and necessary to stimulate SD-like decreases in body, WAT and testes mass? Furthermore, I tested if SD-induced decreases in body fat mass are accompanied by increased energy expenditure, specifically brown adipose tissue (BAT) thermogenesis. It is hoped that the identification of brain sites and mechanisms involved in the effortless reversal of obesity in these animals can be applied to treatment opportunities of human obesity.