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Reproductive effects of SirT1 expression in astrocytes
Author(s) -
Choi Irene Sujeen,
Rickert Emily,
Olefsky Jerry,
Webster Nicholas
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.762.15
Subject(s) - biology , cre recombinase , ovulation , endocrinology , medicine , endocrine system , gene knockdown , hypothalamus , estrous cycle , hormone , adipose tissue , sirtuin 1 , tamoxifen , apoptosis , gene , downregulation and upregulation , transgene , genetically modified mouse , cancer , biochemistry , breast cancer
SirT1 modulates gene‐expression in several organs, including the liver, pancreas, adipose tissue, intestine, and brain. Whereas the impact of SirT1 in these tissues has been shown, its effect on reproduction is still elusive. It has been shown that during times of caloric restriction, SirT1 levels increase and reproductive events such as GnRH pulses, LH pulses, and ovulation cease. We hypothesize that the increase of SirT1 levels in the hypothalamus are the cause of decreased reproductive function. To evaluate this, our laboratory has developed conditional overexpression or knockdown of SirT1 using a tamoxifen‐inducible cre recombinase under the control of the GFAP promoter, which expresses in astrocytes. To prevent any effects on mouse reproductive development, tamoxifen treatment will not be started until 12 weeks of age. We will present data on the reproductive changes by monitoring estrous cyclicity, endocrine and steroid hormone levels, as well as examine fertility of these mice. This research is supported by NIH grants U54HD12303 and T32 DK007494.