title: Higher rates of internal ovulations occur in broiler breeder hens treated with testosterone.
abstract: Maximal profit in both the commercial egg and meat industries requires that the quantity of oviposited eggs closely matches the quantity of large yellow follicles maturing in the ovary. While laying hens are genetically selected for maximal egg production and strategies for management of broiler breeders have been constructed to achieve a similar outcome, a percentage of ovarian follicles that are selected into the ovulatory hierarchy in these hens still never make it to oviposition possibly due to atresia of large yellow follicles or internal ovulation of the oocyte into the peritoneal cavity rather than the oviduct. The causes and mechanisms responsible for these processes remain unclear, however, evidence in wild birds suggests that stressful and/or territorial challenges may stimulate oocyte losses. Since testosterone and corticosterone are central to the responses to territorial intrusions and stress, respectively, and since both large yellow follicles and the oviduct that will engulf them are sensitive to hormonal cues, one or both hormones may play a role in the loss of large yellow follicles via atresia and/or internal ovulation in laying hens. To test this, broiler breeder hens were treated with corticosterone or testosterone 5 h prior to ovulation and observed to see whether these treatments influenced the likelihood that a hen would lay an egg 24 h after the predicted ovulation time. A subset of hens that did not lay an egg were killed and dissected to look for evidence of follicle atresia and internal ovulation. Testosterone treatment resulted in significantly more oocyte losses, and 60% of these occurred due to internal ovulations, as was indicated by the presence of yolk in the peritoneal cavity. Corticosterone did not influence the rate of oocyte losses, follicle atresia, or internal ovulation. These results suggest that testosterone can cause disruptions that ultimately prevent the oviduct from capturing the oocyte after ovulation.
authors.affiliation: Department of Poultry Science, University of Georgia, Athens, GA 30602 USA knavara@uga.edu.
authors.forename: Kristen J
authors.initials: KJ
authors.lastname: Navara
authors.affiliation: Department of Poultry Science, University of Georgia, Athens, GA 30602 USA.
authors.forename: Sara E
authors.initials: SE
authors.lastname: Pinson
authors.affiliation: Livestock Global Discovery, Global Therapeutics Research, Zoetis, 333 Portage Street, KZO 300-535M Kalamazoo, MI 49007 USA.
authors.forename: Parag
authors.initials: P
authors.lastname: Chary
authors.affiliation: Livestock Global Discovery, Global Therapeutics Research, Zoetis, 333 Portage Street, KZO 300-535M Kalamazoo, MI 49007 USA.
authors.forename: Patrick C
authors.initials: PC
authors.lastname: Taube
mesh_terms: D000818:Animals; D002645:Chickens / Q000502:physiology*; D003345:Corticosterone / Q000633:toxicity*; D005260:Female; D005496:Follicular Atresia; D006080:Ovarian Follicle / Q000502:physiology*; D010060:Ovulation / Q000187:drug effects*; D011897:Random Allocation; D013739:Testosterone / Q000633:toxicity*
chemical_list: D013739:Testosterone; D003345:Corticosterone
keywords: atresia; chicken; corticosterone; testosterone