Endocrine Abstracts

Besides its critical functions as a reproductive hormone, 17β-estradiol (E₂), plays an important role in the control of energy homeostasis. In experimental animals, reduction of circulating estrogen levels by bilateral ovariectomy leads to the development of obesity, which can be reversed or prevented by E₂ treatment. E₂ effects on energy balance resemble many similarities to the actions of leptin, key molecule involved in the control of energy homeostasis. In this study, to assess the effects of E₂ in the activation of STAT3 by leptin in the hypothalamus, we used ovariectomized Wistar rats treated with E₂ (OVX +E) or corn oil (OVX), during eight consecutive days. At the eighth day of treatment, they received i.c.v injection (ICV) of leptin or vehicle. We evaluated the phosphorylation of STAT3 protein in the mediobasal hypothalamus (MBH) by Western Blotting or in the hypothalamic nucleus retrochiasmatic (RCA), arcuate (ARC), paraventricular (PVN) and ventromedial (VMN) by the quantification of p- STAT3 positive neurons by immunochemistry. Leptin induced a significant increase in p-STAT3 expression in the MBH, with no difference between OVX e OVX +E groups. Similarly, compared with respective saline group, leptin increased the number of p-STAT3 positive neurons in the RCA, ARC, PVN and VMN of the groups OVX and OVX +E, with no difference between both groups. Interestingly, we observed a higher number of p-STAT3 positive neurons in the VMN of OVX +E rats that received vehicle ICV, compared to OVX rats. These findings suggest that E₂ could act directly in the VMN, activating the STAT3-mediated signaling and this E₂ effect can facilitate leptin actions to reduce body weight and food intake.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details unavailable.