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The implication of the medial preoptic area (MPOA) as a site for estrogen in the regulation of energy balance was investigated. Food intake, O2 consumption (VO2), and CO2 production were measured in ovariectomized rats injected with estradiol (E2) in the medial preoptic nucleus (MPN). Moreover, knowing the potential for corticotropin-releasing factor (CRF) in the anorectic effects of estrogens, we identified estrogen receptors (ER) colocalized in CRF-containing cells of the MPOA and how MPN injections of CRF compared with estrogen injections with respect to VO2 and the VO2-to-CO2 production ratio (respiratory quotient RQ). These energy balance measurements after the injections of four different doses of E2 or CRF were carried out in meal-fed rats chronically implanted with a guide cannula targeted to the MPN. The identification of cells colocalizing ER and CRF was determined using a double-immunostaining procedure revealing ER and CRF immunoreactivities with two different couplers. The injection of E2 into the MPN induced a dose-dependent reduction in food intake, whereas it did not affect VO2 or RQ. Conversely, the injection of CRF into the MPN had no effect on food intake but increased VO2 and decreased RQ. The colocalization of ER and CRF immunoreactivities was found in the MPOA and adjacent regions of the bed nucleus of the stria terminalis. In conclusion, the results of this study provide evidence that the MPOA may represent a potential site for the anorectic effects of E2. Furthermore, the presence of ER and CRF in neurons of the MPOA and adjacent areas suggests a direct interaction between estrogens and the CRF system in the MPOA that is consistent with a role for CRF in the anorectic effects of estrogens. Finally, the results of this study indicate that the effects of a CRF injection into the MPOA differ from those of estrogens, suggesting that if CRF neurons are involved in the anorectic effect of estrogens they likely exert their action outside the MPOA.

The present study was designed to evaluate the interaction of corticosterone (CORT) and female gonadal steroids on energy balance and lipid metabolism. To this end, a 2 x 4 factorial experiment was carried out in which two cohorts of rats differing in their ovary status [OV status: intact (INT) and ovariectomy (OVX)] were each divided into four groups defined by their CORT status [CORT status: nonadrenalectomized (non-ADX), ADX without CORT replacement (placebo subcutaneous pellet), ADX with low-dose CORT replacement, and ADX with high-dose CORT replacement]. After 3 wk of treatment and a 12-h fast, rats were killed and their carcasses analyzed for energy (lipid and protein) content. In addition, indexes of endogenous triglyceride (TRIG) production (liver TRIG content), transport into plasma (triglyceridemia), and incorporation into fat stores [lipoprotein lipase (LPL) activity in adipose tissue (AT)] were assessed. OV and CORT status interacted on body weight gain, total energy, and fat gains. The interactions arose from the fact that the twofold increase in these variables brought on by OVX was abolished by ADX and restored by CORT replacement. Although in ADX groups there was a dose-related restoration of total energy and fat gain by CORT replacement in both INT and OVX cohorts, the impact thereupon of OVX observed in the non-ADX group reappeared only in ADX animals receiving the high dose of CORT. Protein gain was increased by OVX solely in non-ADX rats, whereas the high dose of CORT prevented any net protein gain independently of the OV status. Consistent with treatment effects on total body fat gain, OVX resulted in an increase in liver TRIG content, AT weight, AT LPL activity, and plasma insulin. All these effects of OVX were abolished by ADX and restored by the high dose of CORT. Plasma TRIG were unaffected by OV status but were highly responsive to CORT status. All treatment effects were highly correlated with cumulative food intake. This study shows that the presence of CORT is required for OVX to exert its action on global energy balance and the concomitant, closely integrated adaptations of lipid metabolism.

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