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Submitted on February 2, 2004
Accepted on March 24, 2004
Department of Experimental Pharmacology, *Department of Obstetrics and Gynaecology, University of Naples Federico II, Naples, Italy
* To whom correspondence should be addressed. E-mail: meli{at}unina.it.
Obesity, from declining estrogen levels after menopause, increases the risk of heart disease, diabetes, and hypertension. Ovariectomy in rats is a good model of estrogen insufficiency. The ensuing mild obesity is useful to study how hypoestrogenism alters adiposity. This study aims to examine the hypothesis that in ovariectomized rats modification in estrogen levels or a treatment with a selective estrogen receptor modulator raloxifene (RAL) alters leptinemia and modulates leptin receptor (Ob-R) abundance in hypothalamus and white adipose tissue, in replay to modification of adipose status induced by hypoestrogenism.
Mid- and long-term studies (7 and 22 weeks) were conducted to monitor the change of leptinemia in rats after estrogen loss by ovariectomy (OVX), estrogen replacement by 17-
-estradiol (OVX+E2) or RAL treatment (OVX+RAL). Leptin was significantly higher in OVX rats vs. controls, in a time dependent manner. This effect was reversed both by E2 or RAL treatment at 7 (P < 0.05) and 22 weeks (P < 0.001).
Moreover, E2- or RAL-treatment reverted ovariectomy-induced increase of food intake, body weight and fat mass content; the modifications of serum parameters were examined to evaluate the different lipid profile.
We also evaluated Ob-R expression in hypothalamus and adipose tissue by Western blot analysis. The expression of the long functional isoform (Ob-Rb) increased at 7 weeks only in adipose tissue and decreased at 22 weeks in OVX rats in both tissues and these effects were reversed by E2 or RAL treatment. We provide evidence that central and peripheral Ob-Rb expression is related to modification of estrogen levels.
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