@entity32327 is a potent orexigenic signal and represents a key component of targets through which leptin exerts a regulatory restraint on body adiposity. Part of the orexigenic effects of @entity32327 are mediated by hypothalamic @entity32327 -Y(1) receptors. Here we studied the effect of fasting, leptin, and @entity413 administration on Y(1) receptor gene expression using a transgenic @entity19 model carrying a @entity19 Y(1) receptor/LacZ fusion gene. Transgene expression was determined by quantitative analysis of beta-galactosidase histochemical staining in the paraventricular, arcuate, ventromedial, and dorsomedial hypothalamic nuclei and in the medial amygdala, as a control region. Food deprivation for 72 h decreased transgene expression in the paraventricular nucleus but not in the arcuate nucleus. Leptin treatment, that was per se ineffective, counteracted the decrease of transgene expression induced in the paraventricular nucleus by 72 h fasting. Supplementing the drinking water with 10% @entity413 increased beta-galactosidase expression both in the paraventricular nucleus and arcuate nucleus of control @entity19 . Finally, none of the treatments altered transgene expression in the dorsomedial hyphothalamic, ventromedial, and amygdaloid nuclei. Results suggest that changes in energetic balance affect Y(1) receptor expression in the paraventricular and arcuate nuclei and that leptin regulates the @entity32327 -Y(1) system in the paraventricular nucleus. Different regulatory signals might modulate the @entity32327 -Y(1) transmission in the dorsomedial hyphothalamic and ventromedial hyphothalamic nuclei.

Fasting, leptin treatment, and XXXX administration differentially regulate Y(1) receptor gene expression in the hypothalamus of @entity19 .

@entity19 :: ('10090', 'Species') :: ['mice', 'mouse'] @entity32327 :: ('109648(Tax:10090)', 'Gene') :: ['NPY'] @entity413 :: ('MESH:D005947', 'Chemical') :: ['glucose']
@entity413 :: (MESH:D005947,Chemical) :: ['glucose']
