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Developmental Endocrinology Branch, NICHD, National Institutes of Health, Bethesda, Maryland 20892, USA
1Correspondence: Bldg. 10/10N262, 10 Center Dr., NIH, Bethesda, MD 20892, USA. E-mail: bondyc{at}exchange.nih.gov
Estrogen has many positive effects on neural tissue in experimental
model systems, including stimulation of neurite growth and
neurotransmitter synthesis and protection against diverse types of
neural injury. In humans, estrogen treatment is reputed to protect
against Alzheimer’s disease. To investigate potential mediators of
estrogen’s action and determine whether selective estrogen receptor
modulators (SERMs) such as tamoxifen have estrogen-like effects in the
primate brain, we evaluated the expression of glucose transporters and
insulin-like growth factor 1 (IGF1) and its receptor in the frontal
cortex of ovariectomized rhesus monkeys. We treated one group for 3
days with vehicle, another with 17ß estradiol (E2), and a third with
tamoxifen. The expression of facilitative glucose transporters (Gluts)
1, 3, and 4 was investigated using in situ
hybridization, immunohistochemistry, and immunoblot analysis. Gluts 3
and 4 were concentrated in cortical neurons and Glut1 in capillaries
and glial cells. E2 treatment induced two- to fourfold increases in
Glut3 and Glut4 mRNA levels and lesser but significant increases in
Glut3 and 4 protein levels. E2 treatment induced an 
70%
increase in parenchymal Glut1 mRNA levels, but did not appreciably
affect vascular Glut1 gene expression. IGF1 and IGF1 receptor mRNAs
were concentrated in cortical neurons in a distribution similar to
Gluts 3 and 4. IGF1 mRNA levels were significantly increased in
E2-treated animals but IGF1 receptor mRNA levels were not altered by
hormone treatment. Tamoxifen increased cerebral cortical Glut3 and 4
mRNA levels, but did not affect Glut1, IGF1, or IGF1 receptor
expression. This study provides novel data showing that Gluts 3 and 4
and IGF1 are coexpressed by primate cerebral cortical neurons, where
their expression is enhanced by estrogen. These findings suggest that
up-regulation of glucose transporter and IGF1 expression may contribute
to estrogen’s salutary effects on neural tissue. Tamoxifen, an
antiestrogen at the breast, is shown to have estrogen-like effects on
higher brain centers in the monkey, suggesting that some SERMs may
share estrogen’s neuroprotective potential for menopausal
women.—Cheng, C., Cohen, M., Wang, J., Bondy, C. Estrogen augments
glucose transporter and IGF1 expression in primate cerebral cortex.
Key Words: estradiol • menopause • hormone replacement therapy • Alzheimer’s disease • neurodegeneration
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