Estradiol participates in the control of energy homeostasis, as demonstrated by an increase in food intake and in
body weight gain after
ovariectomy in rats. In the present study, female Wistar rats (200-230 g, N = 5-15 per group), with free access to chow, were individually housed in metabolic cages. We investigated food intake,
body weight, plasma
leptin levels, measured by specific radioimmunoassay, and the hypothalamic
mRNA expression of orexigenic and anorexigenic
neuropeptides, determined by real-time PCR, in ovariectomized rats with (OVX+E) and without (OVX)
estradiol cypionate treatment (10 microg/kg
body weight, sc, for 8 days). Hormonal and
mRNA expression were determined at pre-feeding and 4 h after food intake. OVX+E rats showed lower food intake, less
body weight gain and lower plasma
leptin levels. In the OVX+E group, we also observed a reduction of
neuropeptide Y (NPY),
agouti-related protein (AgRP) and
cocaine- and
amphetamine-regulated transcript (CART)
mRNA expression in the arcuate nucleus and a decrease in
orexin A in the lateral hypothalamic area (LHA). There was an increase in
leptin receptor (LepRb),
melanocortin-4 receptor (MC4-R), CART, and mainly
corticotropin-releasing hormone (CRH)
mRNA in the paraventricular nucleus and LepRb and CART
mRNA in the LHA. These data show that hypophagia induced by
estradiol treatment is associated with reduced hypothalamic expression of orexigenic
peptides such as NPY, AgRP and
orexin A, and increased expression of the anorexigenic mediators MC4-R, LepRb and CRH. In conclusion,
estradiol decreases food intake, and this effect seems to be mediated by peripheral factors such as
leptin and the differential
mRNA expression of
neuropeptides in the hypothalamus.