Document Detail


Effect of melengestrol acetate as an alternative to induce molting in hens on the expression of yolk proteins and turnover of oviductal epithelium.
MedLine Citation:
PMID:  17092663     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Inducing hens to molt increases egg quality, egg production and extends the productive life of hens. It has been previously demonstrated that melengestrol acetate (MGA), an orally active progestin, decreased gonadotropic support for the ovary, which decreased the steroidogenic support for the oviduct and resulted in the cessation of lay. Estradiol produced by the theca cells of small follicles stimulates the production of the yolk proteins vitellogenin II and apolipoprotein II by the liver and supports the oviductal epithelial cells. The objective of the present experiment was to determine gene expression for yolk proteins and oviductal epithelial cell turn-over in response to a MGA-induced molt. Hy-Line W-36 laying hens were fed either 0 or 8mg MGA per day for 28 days in a balanced diet and then returned to a standard layer ration until day 36. Four birds per treatment on days 1, 8, 16, 28 and 36 were euthanized and the liver was removed and snap frozen in liquid nitrogen until RNA was extracted. Expression of vitellogenin II and apolipoprotein II genes was determined using real-time RT-PCR. A portion of the magnum was removed to determine proliferation and programmed cell death for secretory and ciliated luminal epithelium. Vitellogenin II and apolipoprotein II gene expression was reduced in hens fed 8mg MGA compared to those fed 0mg MGA. There was no effect of day on gene expression of either yolk protein. Cell proliferation was increased in the ciliated epithelial cells of the oviduct in hens receiving 8mg MGA compared to those receiving 0mg. However, programmed cell death of the ciliated epithelial cells was not different between controls and MGA treatment. Programmed cell death and proliferation increased in the secretory epithelial cells in hens receiving 8mg MGA compared to controls. Therefore, utilizing MGA as an alternative method to induce molt results in some, but not all, of the physiological changes previously described for hens molted by feed withdrawal. These findings lead us to suggest that some of the observed physiological changes resulting from feed withdrawal are required to increase egg quality and egg production following molt and other changes are not necessary, but are just a result of nutrient deprivation.
Authors:
J M Koch; J S Moritz; D C Lay; M E Wilson
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Publication Detail:
Type:  Controlled Clinical Trial; Journal Article; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2006-09-20
Journal Detail:
Title:  Animal reproduction science     Volume:  102     ISSN:  0378-4320     ISO Abbreviation:  Anim. Reprod. Sci.     Publication Date:  2007 Nov 
Date Detail:
Created Date:  2007-10-23     Completed Date:  2007-12-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7807205     Medline TA:  Anim Reprod Sci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  14-23     Citation Subset:  IM    
Affiliation:
Division of Animal and Veterinary Science, Davis College of Agriculture, Forestry and Consumer Sciences, West Virginia University, Morgantown, WV, United States.
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MeSH Terms
Descriptor/Qualifier:
Animal Feed
Animals
Apolipoproteins / genetics,  metabolism
Apoptosis / drug effects
Cell Proliferation / drug effects
Egg Proteins / genetics*,  metabolism
Epithelial Cells / drug effects
Epithelium / drug effects
Female
Gene Expression Regulation / drug effects*
Glucocorticoids / administration & dosage,  pharmacology
Melengestrol Acetate / administration & dosage,  pharmacology*
Molting / drug effects*
Oviducts / drug effects*,  physiology
Oviposition
Protein Precursors / genetics,  metabolism
Vitellogenins / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Apolipoproteins; 0/Egg Proteins; 0/Glucocorticoids; 0/Protein Precursors; 0/Vitellogenins; 0/apolipoprotein II; 2919-66-6/Melengestrol Acetate

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


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