4.5 Article

Effects of Androgens on Serum Concentrations of Gonadotropins and Ovarian Steroids in Gilts

期刊

BIOLOGY OF REPRODUCTION
卷 79, 期 6, 页码 1148-1152

出版社

OXFORD UNIV PRESS INC
DOI: 10.1095/biolreprod.108.067595

关键词

androgen receptor; androgens; follicle-stimulating hormone; gonadotropins; ovarian steroids; pig

资金

  1. National Research Initiative Competitive [2003-35203-13489]
  2. USDA Cooperative State Research, Education and Extension Service
  3. Ohio Agricultural Research and Development Center
  4. The Ohio State University [4/08AS]

向作者/读者索取更多资源

To examine how androgens affect endocrine events associated with increased ovulation rate, gilts were injected with androgen receptor agonists, an antagonist, or a combination of both. Blood samples were collected hourly from Day 13 to estrus (Day 0 = onset of estrus) coincident with gilts (n = 6 per treatment) receiving daily treatments of vehicle (corn oil), 10 mg of testosterone, 10 mg of 5 alpha-dihydrotestosterone (dihydrotestosterone), 1.5 g of flutamide (an androgen receptor antagonist), testosterone plus flutamide, or dihydrotestosterone plus flutamide. Treatment of gilts with testosterone or dihydrotestosterone alone increased (P < 0.05) concentrations of FSH in serum, and these effects were blocked by cotreatment with flutamide. Estradiol-17beta and androstenedione concentrations in serum were increased (P < 0.05) at 2 h after injection of testosterone or testosterone plus flutamide but not after dihydrotestosterone treatment, probably because of the role of testosterone as a substrate for estradiol-17beta and androstenedione synthesis. There were no effects of the six treatments on serum concentrations of progesterone during luteolysis, but treating gilts with testosterone shortened (P < 0.05) the proestrous period. Total embryonic loss by Day 11 in gilts treated with dihydrotestosterone was reversed when gilts were cotreated with dihydrotestosterone plus flutamide. Results of this experiment indicated that androgen actions both increased FSH secretion and reduced embryonic survival by a mechanism(s) dependent on the androgen receptor.

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