Administration of testosterone from day 13 of the estrous cycle to estrus increased the number of corpora lutea and conceptus survival in gilts.

Abstract

The effects of exogenous androgens on the number of corporea lutea (CL) and conceptus survival were examined in crossbred gilts. In Exp. 1, gilts received 1 mg of testosterone per day from d 13 (d = 0 first day of estrus, n = 21) or d 16 until estrus (n = 23). Gilts in the vehicle group received corn oil (n = 20). Gilts were mated and on d 11.5 their concepti and CL were evaluated. In Exp. 2, conceptus survival was examined at the 4- to 8-cell, early blastocyst or hatching blastocyst stages for gilts given vehicle or 1 mg testosterone from d 13 (24 gilts per group). In Exp. 3, gilts received 1 mg of androstenedione (n = 20) or vehicle (n = 18) per day from 13 d to estrus and then were mated and evaluated on d 11.5. Results from Exp. 1 indicated that the number of CL was greater (P < .04) in gilts treated with testosterone from d 13 to estrus than in gilts receiving vehicle (16.4 vs 14.8, respectively). Similarly, the number (P < .01) and recovery rate (P < .04) of blastocysts were greater in gilts treated with testosterone from d 13 to estrus than in gilts treated with testosterone from d 16 to estrus in gilts receiving vehicle (number, 15.3 vs 12.8 or 12.8; recovery rate, 95 vs 87 or 86%, respectively). Gilts treated testosterone or vehicle did not exhibit differences (P > .05) in number of normal concepti at the 4- to 8-cell and hatching stages. However, prior treatment with testosterone delayed conceptus death; gilts treated with testosterone had more (P < .01) normal concepti at the intermediate stage (early blastocyst) than those treated with vehicle (treatment x embryo stage interaction, P < .05). In Exp. 3, androstenedione treatment did not influence (P > .10) the number of CL or the number and recovery rates of d-11.5 blastocysts. Treating gilts with testosterone from d 13 of the estrous cycle to the following estrus increased the number of CL and blastocyst survival, perhaps by improving some, as yet unknown, aspect(s) of oocyte quality.