Mol. Hum. Reprod. Advance Access originally published online on May 21, 2004
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Molecular Human Reproduction, Vol. 10, No. 7, pp. 473-479, 2004
Molecular Human Reproduction vol. 10 no. 7 © European Society of Human Reproduction and Embryology 2004; all rights reserved
Selective alterations in insulin receptor substrates-1, -2 and -4 in theca but not granulosa cells from polycystic ovaries
1Department of Obstetrics and Gynecology, Cedars–Sinai Burns and Allen Research Institute, Cedars–Sinai Medical Center/The David Geffen School of Medicine at UCLA, 8700 Beverly Blvd., Davis 2066, Los Angeles, CA 90048, USA 2Department of Obstetrics and Gynecology, 2nd Clinic of Surgical Gynecology, University School of Medicine, 8 Jaczewski Street, 20-090 Lublin, Poland
3 To whom correspondence should be addressed. Email: magoffin{at}cshs.org
The elevated insulin concentrations that occur in many women with polycystic ovary syndrome (PCOS) can contribute significantly to ovarian hyperandrogenism. The objective of the present study was to compare the content of proximal insulin signalling molecules in theca and granulosa cells between polycystic ovaries and regular cycling controls. Individual follicles 
were obtained from 11 women with PCOS and 10 regularly cycling control women. The theca and granulosa cells were microdissected from each follicle. Total protein was extracted and signalling proteins were measured by western blot analysis. There was no difference in insulin receptor content between PCOS and controls in either theca or granulosa cells. Insulin receptor substrate (IRS)-1 and -2 were increased 
but IRS-4 was decreased 
in PCOS theca cells. There were no changes in IRS-1, -2 or -4 in granulosa cells. IRS-3 was undetectable in all samples. There were no changes in phosphatidyl inositol-3 kinase catalytic subunits p110
or p110ß in either theca or granulosa cells. These data demonstrate cell-specific alterations in IRS protein concentrations in theca cells from polycystic ovaries that are consistent with an exaggerated amplification of the insulin signal and which may play an important role in ovarian hyperandrogenism and thecal hyperplasia.
Key words: granulosa cell/insulin receptor substrate/insulin signalling/PCOS/theca cell
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