Document Detail

Effect of glucocorticoid-induced insulin resistance on follicle development and ovulation.
MedLine Citation:
PMID:  23616591     Owner:  NLM     Status:  MEDLINE    
Polycystic ovarian syndrome (PCOS) is characterized by hyperandrogenemia, polycystic ovaries, and menstrual disturbance and a clear association with insulin resistance. This research evaluated whether induction of insulin resistance, using dexamethasone (DEX), in a monovular animal model, the cow, could produce an ovarian phenotype similar to PCOS. In all of these experiments, DEX induced insulin resistance in cows as shown by increased glucose, insulin, and HOMA-IR (homeostasis model assessment of insulin resistance). Experiment 1: DEX induced anovulation (zero of five DEX vs. four of four control cows ovulated) and decreased circulating estradiol (E2). Experiment 2: Gonadotropin-releasing hormone (GnRH) was administered to determine pituitary and follicular responses during insulin resistance. GnRH induced a luteinizing hormone (LH) surge and ovulation in both DEX (seven of seven) and control (seven of seven) cows. Experiment 3: E2 was administered to determine hypothalamic responsiveness after induction of an E2 surge in DEX (eight of eight) and control (eight of eight) cows. An LH surge was induced in control (eight of eight) but not DEX (zero of eight) cows. All control (eight of eight) but only two of eight DEX cows ovulated within 60 h of E2 administration. Experiment 4: Short-term DEX was initiated 24 h after induced luteal regression to determine if DEX could acutely block ovulation before peak insulin resistance was induced, similar to progesterone (P4). All control (five of five), no P4-treated (zero of six), and 50% of DEX-treated (three of six) cows ovulated by 96 h after luteal regression. All anovular cows had reduced circulating E2. These data are consistent with DEX creating a lesion in hypothalamic positive feedback to E2 without altering pituitary responsiveness to GnRH or ovulatory responsiveness of follicles to LH. It remains to be determined if the considerable insulin resistance and the reduced follicular E2 production induced by DEX had any physiological importance in the induction of anovulation.
Katherine S Hackbart; Pauline M Cunha; Rudelle K Meyer; Milo C Wiltbank
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-06-20
Journal Detail:
Title:  Biology of reproduction     Volume:  88     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2013 Jun 
Date Detail:
Created Date:  2013-06-21     Completed Date:  2013-10-21     Revised Date:  2014-07-01    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  153     Citation Subset:  IM    
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MeSH Terms
Blood Glucose
Dexamethasone / pharmacology*
Estradiol / blood
Glucocorticoids / pharmacology*
Gonadotropin-Releasing Hormone / pharmacology
Hypothalamus / drug effects,  secretion
Insulin Resistance / physiology*
Luteinizing Hormone / blood,  secretion
Ovarian Follicle / drug effects*,  growth & development
Ovulation / drug effects*
Progesterone / pharmacology
Grant Support
Reg. No./Substance:
0/Blood Glucose; 0/Glucocorticoids; 33515-09-2/Gonadotropin-Releasing Hormone; 4G7DS2Q64Y/Progesterone; 4TI98Z838E/Estradiol; 7S5I7G3JQL/Dexamethasone; 9002-67-9/Luteinizing Hormone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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