During the last five years it has been well established that photoperiod induced changes in body weight in the seasonal hamster, Phodopus sungorus, are accompanied by a marked seasonal cycle in leptin sensitivity. In the current study we investigated the possible involvement of insulin signaling in seasonal body weight regulation. We analyzed the expression pattern and relative intensity of insulin receptor (IR), Pi3-Kinase (Pi3K) and protein tyrosine phosphatase 1B (PTP1B) mRNAs by in situ hybridization in the brains of juvenile female hamsters acclimated to either long (LD) or short day-length (SD) for eight weeks, with or without superimposed food deprivation for 48h. Furthermore, the hypothalamic concentration and distribution of phospho-AKT, a marker of Pi3K activity was determined by immunoblotting and immunohistochemistry. Eight weeks acclimation to SD led to a substantial downregulation of IR, PTP1B gene expression and phospho-AKT concentration in this brain region, whereas Pi3K mRNA was unchanged. Food deprivation induced a decrease in PTP1B and a trend towards lowered IR gene expression in LD but not in SD. Additionally, a striking increase in PTP1B gene expression in the thalamus was observed after food deprivation in both photoperiods. The direction of change in neuronal insulin signaling contrasts to the central catabolic nature of this pathway described in other species. SD-induced reduction in insulin signaling may be due to the decline in body fat stores mediated by enhanced central leptin sensitivity. The increased anorexigenic tone of leptin may overwrite central insulin signaling to prevent catabolic overdrive.