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University of Wisconsin, Madison 53706
4 Address for reprint requests: Department of Meat and Animal Science, University of Wisconsin, Madison 53706.
Abstract
One hundred and two puberal gilts from nine genetic groups were used to determine the association of two morphological types of ovarian follicular loss (hemorrhagic and milky) with genetic background of gilts, level of feed intake and stage of estrous cycle. At estrus (day 0 of estrous cycle) a lesser proportion of gilts (P<.05) had hemorrhagic follicles than gilts at day-15. While the total number of follicles decreased from day-15 to estrus (P<.01), the proportion of milky follicles increased (P<.01). No milky follicle was larger than 6 mm in diameter. The high level of feed intake increased (P=.06) the number of large follicles (7 to 10 mm), their average mean diameter (P<.05) and the proportion of gilts with hemorrhagic follicles (P<.05). Although the proportion of milky follicles did not differ significantly between the feed groups, the regression of the average number of large follicles on the average percent milky was negative (.26) and suggested that full-feeding increased the number of preovulatory follicles through a lessened amount (though small) of atresia.
Poland China gilts lost fewer (P<.05) follicles between day-15 and estrus than Hampshire or Yorkshire gilts and had the fewest milky follicles (P<.05). Full-feeding increased the mean diameter of follicles in Poland China gilts but had little effect on the follicular diameter of the other pure breeds (P<.05). Differences between some of the reciprocal crossbred pairs were found in the total number of follicles, the number of large follicles and the proportion of milky follicles.
1 This work was done under a cooperative agreement between the Research Division of the College of Agricultural and Life Sciences, University of Wisconsin, and the Animal Husbandry Research Division, A.R.S., U.S.D.A., and supported in part by Cooperative U.S.D.A. C.S.R.S., Grants No. 816-15-20 and 916-15-02. It was also supported in part by the Ford Foundation, Grant No. 63-505, by the Program Project in Genetics, Grant No. GM 15422, from the National Institutes of Health and by the Public Health Service Training Grant No. 5-TO1 HD00104-09. This paper is No. 641 from the Department of Meat and Animal Science and No. 1745 from the Laboratory of Genetics.
2 Present address: Department of Physiology, Emory University, Atlanta, GA 30322.
3 Present address: Wisconsin Regional Primate Research Center, University of Wisconsin, Madison 53706.
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