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Am J Physiol Regul Integr Comp Physiol 291: R643-R650, 2006. First published April 6, 2006; doi:10.1152/ajpregu.00807.2005
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Photoperiodic regulation of insulin receptor mRNA and intracellular insulin signaling in the arcuate nucleus of the Siberian hamster, Phodopus sungorus

Alexander Tups,1,2 Michael Helwig,1,2 Sigrid Stöhr,2 Perry Barrett,1 Julian G. Mercer,1 and Martin Klingenspor2

1Division of Obesity and Metabolic Health, Rowett Research Institute, Aberdeen Centre for Energy Regulation and Obesity, Aberdeen, Scotland, and 2Department of Animal Physiology, Philipps University Marburg, Marburg, Germany

Submitted 15 November 2005 ; accepted in final form 25 March 2006

During the last 5 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 present 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), phosphatidylinositol 3-kinase (PI3-kinase), 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 8 wk, with or without superimposed food deprivation for 48 h. Furthermore, the hypothalamic concentration and distribution of phospho-AKT, a marker of PI3-kinase activity was determined by immunoblotting and immunohistochemistry. Eight weeks of acclimation to SD led to a substantial downregulation of IR, PTP1B gene expression, and phospho-AKT concentration in this brain region, whereas PI3-kinase mRNA was unchanged. Food deprivation induced a decrease in PTP1B and a trend toward 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 decline in body fat stores mediated by enhanced central leptin sensitivity. Increased anorexigenic tone of leptin may overwrite central insulin signaling to prevent catabolic overdrive.

protein tyrosine phosphatase 1B; body weight regulation; hypothalamus; thalamus



Address for reprint requests and other correspondence: A. Tups, Dept. of Animal Physiology, Philipps Univ. Marburg, Karl von Frisch Str. 8, D-35043 Marburg, Germany (e-mail: tups{at}staff.uni-marburg.de)







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