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Association of insulin with aspects ...

The University of Wisconsin - Madison.

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Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome./
作者:	Zhou, Rao.
面頁冊數:	331 p.
附註:	Adviser: David H. Abbott.
Contained By:	Dissertation Abstracts International69-09B.
標題:	Agriculture, Animal Pathology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3327845
ISBN:	9780549800965

Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome.
Zhou, Rao.

Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome. - 331 p.

Adviser: David H. Abbott.

Thesis (Ph.D.)--The University of Wisconsin - Madison, 2008.

This thesis describes several studies designed to improve our understanding of reproductive dysfunction, adrenal hyperandrogenism, and the consequence of insulin resistance in prenatally androgenized (PA) female monkeys, a model for polycystic ovary syndrome (PCOS). The first study characterized how fetal androgen excess during early gestation diminishes ovulatory frequency, compromises luteal phase function, and induces hyperandrogenism. These findings resemble the symptoms of PCOS women who undergo menstrual cycles; luteal phase defects may precede the onset of chronic anovulation.

ISBN: 9780549800965Subjects--Topical Terms:

1021764
Agriculture, Animal Pathology.

Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome.
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100 1 $a Zhou, Rao. $3 1031149
245 1 0 $a Association of insulin with aspects of adrenal and ovarian dysfunction in a nonhuman primate model of polycystic ovary syndrome.
300 $a 331 p.
500 $a Adviser: David H. Abbott.
500 $a Source: Dissertation Abstracts International, Volume: 69-09, Section: B, page: .
502 $a Thesis (Ph.D.)--The University of Wisconsin - Madison, 2008.
520 $a This thesis describes several studies designed to improve our understanding of reproductive dysfunction, adrenal hyperandrogenism, and the consequence of insulin resistance in prenatally androgenized (PA) female monkeys, a model for polycystic ovary syndrome (PCOS). The first study characterized how fetal androgen excess during early gestation diminishes ovulatory frequency, compromises luteal phase function, and induces hyperandrogenism. These findings resemble the symptoms of PCOS women who undergo menstrual cycles; luteal phase defects may precede the onset of chronic anovulation.
520 $a The second study investigated whether menstrual function improved after insulin sensitivity was enhanced by pioglitazone treatment. Pioglitazone normalized menstrual cycles and luteal phase defects in 62% of PA females without affecting normal cycles in control females. Pioglitazone also diminished serum progesterone, and increased estradiol responses to hCG stimulation. These findings suggest insulin resistance may play a causal role in maintaining ovulatory dysfunction in PA monkeys.
520 $a The third study examined whether hyperinsulinemia could exaggerate luteal phase defects and ovulatory dysfunction in PA female monkeys with normal circulating insulin levels. After daily insulin or placebo subcutaneous injections for 6-7 months, duration of the follicular phase was normalized in PA monkeys. There was no evidence of insulin-induced ovarian hyperandrogenism or excessive LH secretion. These results suggest that hyperinsulinemia fails to induce hyperandrogenic anovulation. Insulin may instead act as a co-gonadotropin.
520 $a The fourth study determined whether adrenal androgen excess was manifest in female PA monkeys. Serum levels of DHEA in PA females exceeded those in controls before and after dexamethasone (Dex)-ACTH administration. After ACTH injection, PA females exhibited higher serum levels of DHEA, androstenedione, and corticosterone. These results reflect up-regulation of 17,20 lyase activity in the adrenal zona reticularis, causing adrenal androgen excess comparable to that found n PCOS women.
520 $a The fifth study determined adrenal steroid responses to Dex-ACTH after increasing insulin sensitivity through pioglitazone administration, and increasing circulating insulin levels by subcutaneous insulin injections. Pioglitazone decreased DHEAS response to Dex-ACTH, while no changes were detected in the insulin study. Overall, these studies established insulin resistance-related menstrual, ovarian and adrenal dysfunction and in a nonhuman primate model for PCOS.
590 $a School code: 0262.
650 4 $a Agriculture, Animal Pathology. $3 1021764
650 4 $a Health Sciences, Obstetrics and Gynecology. $3 1020690
650 4 $a Health Sciences, Pathology. $3 1017854
690 $a 0380
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710 2 $a The University of Wisconsin - Madison. $3 626640
773 0 $t Dissertation Abstracts International $g 69-09B.
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790 1 0 $a Abbott, David H., $e advisor
791 $a Ph.D.
792 $a 2008
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