LEPTIN (OB) MESSENGER-RNA AND HYPOTHALAMIC NPY IN FOOD-DEPRIVED REFEDSYRIAN-HAMSTERS/

Food deprivation in the laboratory rat decreases plasma leptin and ins ulin, elevates glucocorticoid concentration, and increases the activit y df the neuropeptide Y (NPY) system and feeding drive. In contrast, S yrian hamsters fail to modify feeding behaviour in response to various food scarcity paradigms. Two components of the neuroendocrine-hormona l response to food deprivation, adipose tissue-derived leptin and hypo thalamic NPY, are investigated in the Syrian hamster, ob (leptin) mRNA was less abundant in subcutaneous than abdominal adipose tissue, but not to the extent observed in other rodents. Food deprivation for 48 h reduced ob mRNA in inguinal and retroperitoneal white adipose tissue; gene expression was partially restored by refeeding. In contrast, in epididymal fat there was no effect on ob mRNA. NPY concentrations in h ypothalamic nuclei were also unaffected by feeding state. The predicte d amino acid sequence of leptin from the Syrian hamster was over 90% h omologous with Djungarian hamster and mouse sequences, and the leptin receptor gene (OB-R), and specifically the long intracellular splice v ariant, OB-Rb, was expressed in the same forebrain and hypothalamic re gions that have been described in laboratory mice and rats, including hypothalamic arcuate, dorsomedial, and ventromedial nuclei. The failur e of food deprivation to affect NPY and feeding behaviour in Syrian ha msters is unlikely to be due to defects in the leptin system, although there may be region-specific differences in the relation of leptin si gnaling in laboratory rats and Syrian hamsters. (C) 1998 Elsevier Scie nce Inc.