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Chronic Estradiol Treatment Improves Brain Homeostasis during Aging in Female Rats

Department of Functional Biology (A.A., M.M., P.O., R.F., F.D., C.G.), Physiology Area, and Department of Morphology and Cellular Biology (C.P., A.N., J.T.), University of Oviedo, 33006 Oviedo, Spain

Address all correspondence and requests for reprints to: Dr. Celestino González, Assistant Professor of Physiology, Department of Functional Biology, Physiology Area, University of Oviedo, C/Julián Clavería s/n 33006, Oviedo, Spain. E-mail: tinog{at}uniovi.es.

Aging is associated with a reduction in metabolic function, insulin resistance, increased incidence of neurodegenerative diseases, and memory or cognitive dysfunction. In aging females, loss of gonadal function determines the beginning of the period of reduced metabolic function. Estrogens have neuroprotective effects, but the mechanisms by which they exert these effects remain unclear. The effects of estradiol treatment on the activation of the insulin receptor substrate (IRS)-1 signaling pathway, the interactions between estrogen receptor (ER)- and IRS-1 and the p85 subunit of phosphatidylinositol-3 kinase, together with the possible effects of estradiol treatment on glucose transporter-3 and -4 levels, were investigated in female rats. The level of expression of each glucose transporter was greater in control and estradiol-treated groups than in the ovariectomized group. Interactions of ER46-IRS-1, ER46-p85, and p85-IRS-1, as well as IRS-1 phosphorylation, appeared to increase with estradiol treatment. The results indicate that estradiol treatment improves some aspects of neuronal homeostasis that are affected by aging; this may indicate that estradiol has neuroprotective effects in female rats. Additional animal studies are required to clarify the neuroprotective role of estradiol in relation to other important molecules involved in the IRS-1-phosphatidylinositol-3 kinase signaling pathway.