Beverly Hutcherson
Campus Address: Room 260, 1220 Capitol Court, Madison, WI 53715
Telephone: (608) 265-4854
Major Professor: Dr. David Abbott
Email: bahutcherson@wisc.edu
Degree Goal: M.S.
Background: B.S. 2003, Marquette University, Biology
Current research: Polycystic ovary syndrome (PCOS) is a complex human disorder of unknown etiology. It is the leading cause of anovulation and type 2 diabetes in young women. Prenatal androgen access may be the cause of reprogramming of multiple organ systems including the ovary. Our lab is concerned with investigating the underlying mechanism of the reproductive and metabolic origins of PCOS using a non-human primate model for the syndrome. Women with PCOS have high rates of miscarriage even after in vitro fertilization cycles. This alludes to a problem within the follicle. It has been shown that these prenatally androgenized rhesus females suffer from an LH hypersecretory environment. They also respond to recombinant hCG-induced luteinization in an exaggerated way. This exaggerated response may be due to an alteration in ovarian response to gonadotropin stimulation. In my thesis, I seek to investigate, through molecular techniques, the LH receptor’s role in granulosa cell dysfunction in folliclular response to recombinant hCG-induced luteinization as part of an ovarian hyperstimualtion protocol for in vitro fertilization (IVF).
Awards: Advanced Opportunity Fellow 2003-2004
Presentations (poster):
Hutcherson, B.A., Bruns, C.M., Goodfriend, T.L., Abbott, D.H. 2004. Association between free fatty acids and insulin resistance in a nonhuman primate model for polycysic ovary syndrome. Abtract no.18, Annual ERP Symposium, October 15, 2004, Madison, WI, USA
Hutcherson, B.A., Bruns, C.M., Goodfriend, T.L., Abbott, D.H. 2004. Association between free fatty acids and insulin resistance in a nonhuman primate model for polycysic ovary syndrome. Abtract no. P39, Center for Reproductive Science, 25 th Annual mini-symposium on Reproductive Biology, October 18, 2004, Evanston, IL, USA