J. Anim Sci.
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J. Anim Sci. 1988. 66:3208-3217.
© 1988 American Society of Animal Science

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Postpartum Reproduction in Protein Restricted Beef Cows: Effect on the Hypothalamic-Pituitary-Ovarian Axis1,2,

C. J. Nolan3,4,, R. C. Bull3,5,, R. G. Sasser3, C. A. Ruder3, P. M. Panlasigui3, H. M. Schoeneman6,7, and J. J. Reeves7

University of Idaho, Moscow 83843

Abstract

The influence of dietary CP on circulating LH and anterior pituitary and hypothalamic function was examined. In Exp. 1, 28 cows were randomly assigned to four treatment groups: adequate CP (ADQ; .96 kg/d) or deficient CP (DEF; .32 kg/d) beginning at 90, 60 and 30 d before parturition and continued at a 33% increase in feed consumption after parturition. Cows were bled at 15-min intervals for 8 h on d 20, 40 and 60 after parturition. Pituitaries were collected on d 62 to analyze GnRH receptor numbers and gonadotropin content. Frequency of pulsatile LH release increased (P < .05) from 20 to 60 d in ADQ cows. Basal and mean LH were not affected (P > .10) by CP restriction or by days after parturition. Crude protein did not affect pituitary GnRH receptors (P > .10), but it did affect pituitary LH content, FSH content and FSH concentration (P < .05). In Exp. 2, 28 cows were assigned to treatment groups as in Exp. 1. All cows were challenged with GnRH (.22 µg/kg BW) at 20, 40 and 60 d after parturition and were bled every 30 min for 6 h. Responsiveness to GnRH increased with increased time after parturition (P < .07). Deficient CP decreased GnRH-induced LH release (P < .05). In Exp. 3, 12 cows were randomly assigned to ADQ or DEF CP beginning 120 d before parturition. All cows received 1 mg estradiol-17ß (E2) on d 19, 39 and 59 after parturition and were bled every 30 min for 14 h beginning 14 h following E2. Response to E2 was unaffected by CP restriction (P > .10), whereas time to E2-induced LH peak decreased as time after parturition increased in ADQ cows (P < .05). Results suggest that delayed return to estrus in CP-deficient postpartum beef cows might be due to reduced gonadotropin release from the anterior pituitary and decreased anterior pituitary responsiveness to GnRH.


Footnotes

1 Idaho Agric. Exp. Sta. Publ. No. 8744.

2 The authors gratefully acknowledge L. E. Reichert, Jr. for purified LH, J. A. Dias for FSH antibody and J. W. Paul and J. Sandow of Hoescht A. G. For GnRH analog.

3 Dept. of Anim. Sci.

4 Present address: Steroid Research Unit, Dept. of Obstetrics and Gynecology, Women's Hospital L1221-0278, Univ. of Michigan, Ann Arbor 48109-0278.

5 To whom reprint requests should be sent.

6 Present address: Dept. of Medicine, Uniformed Services Univ. of Health Sciences, Bethesda, MD 20814.

7 Dept. of Anim. Sci., Washington State Univ., Pullman 99164.







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Copyright © 1988 by the American Society of Animal Science.