Estradiol feedback inhibition of luteinizing hormone concentrations in the anestrous sow

The suppressive effects of exogenous 17 beta-estradiol (E2) on LH concentrations in sows that remained anestrus following weaning and in those that returned to estrus were evaluated. Four anestrous and four cyclic sows were treated subcutaneously with silastic implants containing E2 at 13 d after ovariectomy (d 0). Three anestrous and six cyclic sows received silastic implants without E2. Blood was collected at 6-h intervals from d -1 to d 12 and at 15-min intervals for 8 h on d -1, 2, 7 and 12. Sows were treated with 1 microgram GnRH/kg BW at the completion of each 8-h frequent sampling period. Blood was collected at intervals of 10 to 30 min for 3 h after GnRH treatment. Concentrations of E2 remained less than 5 pg/ml in sham-treated sows and were between 20 and 25 pg/ml in E2-treated females. Pulsatile LH concentrations was similar between anestrous and cyclic sows prior to implant treatment. Sham-treated anestrous sows had greater (P less than .05) pulse frequency and mean LH concentrations than E2-treated anestrous sows on d 2, 7 and 12. Differences in pulsatile LH concentrations between E2-treated and sham-treated cyclic sows were not detected. Pulse frequency was less (P less than .05) in E2-treated anestrous sows than in E2-treated cyclic sows on d 7 and 12. Peak LH concentrations were greater (P less than .05) in E2-treated cyclic sows than in E2-treated anestrous sows at each GnRH challenge. These results suggest that the hypothalamo-hypophyseal axis is more sensitive to the negative feedback effects of E2 in anestrous sows than in cyclic sows. In addition, chronic E2 treatment reduces pituitary responsiveness to GnRH to a greater extent in anestrous than in cyclic sows. Failure to return to estrus in swine may be due, at least in part, to an increased sensitivity of the hypothalamo-hypophyseal axis to the negative feedback effect of estradiol.     

The influence of ovariectomy on luteinizing hormone concentrations in anestrous and cyclic sows

In an effort to determine whether anestrus in swine is due to aberrant ovarian feedback control of gonadotropin release, this study contrasted the influence of ovariectomy on LH concentrations in serum of anestrous sows and in sows that returned to estrus following weaning. Blood samples were collected at 6-h intervals from 7 d prior to until 4 d after ovariectomy of 22 anestrous and 24 cyclic sows. Blood samples also were collected at 15-min intervals for 8 h at 2 d prior to and 2 d after ovariectomy. Sampling at 6-h intervals continued until 12 d after ovariectomy and additional 8-h windows of 15-min samples were taken at 7 and 12 d after ovariectomy of seven anestrous and nine diestrous sows. Mean LH concentrations and LH pulse frequencies were greater (P less than .05) 2 d after ovariectomy than 2 d prior to ovariectomy in both anestrous and diestrous sows. Mean pulse amplitude had increased by 2 d after ovariectomy in anestrous sows but did not change in cyclic sows. Baselines as determined from the mean of all LH measurements excluding pulses, remained the same in both anestrous and diestrous sows at 2 d after ovariectomy. Pulse frequency, pulse amplitude, and mean LH concentration were greater (P less than .05) in both anestrous and diestrous sows at 7 and 12 d after ovariectomy than at 2 d prior to and 2 d after ovariectomy. Pulse amplitude on d 7 and 12 after ovariectomy decreased (P less than .05) in both anestrous and diestrous sows relative to those observed at earlier times.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of exogenous estradiol-17 beta on luteinizing hormone, progesterone, and estradiol-17 beta concentrations before and after prostaglandin F2 alpha-induced termination of pregnancy and pseudopregnancy in gilts.

This study evaluated the influence of exogenous estradiol-17 beta (E2) administration on LH concentrations and the number of animals returning to estrus after the termination of pregnancy or pseudopregnancy in gilts. Gilts were mated (pregnant; n = 11) on the 1st d of estrus or received 5 mg of estradiol valerate i.m. at d 11 to 15 after the onset of estrus (pseudopregnant; n = 9). Gilts were treated with prostaglandin F2 alpha (PGF2 alpha, 15 and 10 mg) at 12-h intervals on d 44 of pregnancy or pseudopregnancy. The day of abortion or luteolysis (progesterone less than .2 ng/mL) was considered d 0. Six pregnant and four pseudopregnant gilts received s.c. an E2 capsule (24 mg of E2) on d -20 and additional E2 capsules on d -13 and -6. The E2 capsules were removed on the day after PGF2 alpha administration. Blood samples were collected at 12-h intervals from d -21 to -3, at 6-h intervals from d -2 to 21 or the onset of estrus, and at 15-min intervals for 8 h on d -2, 1, 4, 7, 10, 14, and 18. After each 8-h sampling period, gilts were treated i.v. with GnRH at .5 micrograms/kg of BW and blood samples collected at 10-min intervals for 3 h. A greater (P less than .05) proportion of sham-treated gilts than of E2-treated gilts exhibited a preovulatory-like LH surge after abortion/luteolysis. It was evident that E2 supplementation before luteolysis reduced the ability of pregnant and pseudopregnant gilts to return to estrus.     

Effects of chronic gonadotropin-releasing hormone agonist treatment on serum luteinizing hormone and testosterone concentrations in boars.

Mature boars were subjected to chronic treatment with a gonadotropin-releasing hormone (GnRH) agonist, goserelin (D-Ser[But]6, Azgly-NH210), and serum luteinizing hormone (LH) and testosterone concentrations were measured. Ten sexually mature boars were randomly assigned to treatment (n = 5) or control (n = 5) groups. On day 0, boars were implanted sc (day 0) with 2 GnRH agonist implants (1 mg of GnRH/implant) or sham implants. Blood samples were collected at 12-hour intervals on days -2 and -1, at 6-hour intervals on days 0 through 4, and at 12-hour intervals on days 5 through 8. In addition, blood samples were collected at 15-minute intervals for 6 hours on days -1, 0, 4, and 8. Serum testosterone and LH concentrations were determined by radioimmunoassay. Maximal LH (7 +/- 1 ng/ml) and testosterone (26 +/- 3 ng/ml) concentrations were observed at 5 and 18 hours, respectively, after GnRH agonist treatment. Subsequently, LH and testosterone concentrations decreased to pretreatment values (0.3 +/- 0.1 ng/ml and 1.8 +/- 0.4 ng/ml, respectively) by 24 and 48 hours, respectively, after GnRH agonist implantation. Few differences in the characteristics of pulsatile LH release were observed between the groups. Testosterone and LH concentrations in samples collected at 6- and 12-hour intervals and pulsatile LH release did not change after sham treatment of control boars. Whereas previous reports indicated that chronic GnRH administration suppressed serum LH and testosterone concentrations in rams, rats, and dogs, our results indicate that chronic GnRH agonist treatment induced transitory increases, without subsequent suppression, in LH and testosterone concentrations in mature boars.     

Effects of estradiol-17 beta, naloxone and gonadotropin releasing hormone on postpartum secretion of luteinizing hormone in fall-lambing ewes

The interaction among exogenous estradiol-17 beta, naloxone and gonadotropin releasing hormone (GnRH) in the control of luteinizing hormone (LH) secretion was studied in intact postpartum ewes nursing their offspring. One-half of 30 fall-lambing ewes were implanted subcutaneously with an estradiol-17 beta containing Silastic capsule between postpartum d 1 and 12 which doubled their serum concentrations of estradiol (16.0 +/- .1 vs 8.4 +/- .1 pg/ml). Blood samples were collected from implanted and non-implanted ewes at 15-min intervals for 5 h on d 3, 8, 13, 20 and 28 postpartum. Pre-injection samples were collected for 1 h, and ewes were injected with saline, naloxone (NAL;1 mg/kg) or GnRH (100 micrograms/ewe). When averaged across all days and implant groups, serum LH in the three post-NAL samples was higher (P less than .05) than in the three pre-NAL samples (3.6 +/- 1.2 vs .6 +/- .2 ng/ml). Post-GnRH concentrations of serum LH were lower (P less than .05) in estradiol-implanted ewes than in non-implanted ewes on d 8 and 13, but there were no differences in any LH characteristics on d 20 and 28 after implant removal on d 12. In non-implanted ewes, serum LH responses to GnRH increased (P less than .05) eightfold from d 3 (3.8 +/- 1.4 ng/ml) to d 8 (31.6 +/- 1.4 ng/ml), remained elevated through d 20, but declined by d 28 (10.8 +/- 1.4 ng/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

Gonadotropin-releasing hormone-induced luteinizing hormone release in heifers: effect of nutrition during gestation

The effects of nutrition during the last two trimesters of gestation on GnRH-induced LH release were assessed in crossbred heifers. Heifers (n = 58) were allotted at 90 d gestation to one of three levels of an experimental diet fed at 1, 1.5 or 2% of BW to attain maternal BW loss, BW maintenance or BW gain, respectively, at parturition. Twenty-two heifers were injected (i.m.) once with 100 micrograms GnRH between d 14 and 1 before parturition, and 32 heifers were injected (i.m.) once with 100 micrograms GnRH between d 8 and 21 after parturition. Jugular blood samples were collected before and at 30-min intervals after GnRH for 4 h. Least squares means for BW change differed (P less than .01) among BW loss (-17.6%), BW maintenance (-6.0%) and BW gain (7.0%) heifers. Basal plasma LH concentration was not influenced by nutritional treatment and was similar before and after parturition for all groups. However, in response to GnRH, peak plasma LH concentration was greater (P less than .10) for prepartum than for postpartum heifers. Mean LH peak amplitude in prepartum heifers was approximately twofold greater (P less than .10) in the BW loss and maintenance groups compared with the BW gain group. Prepartum LH release was related inversely (r = -.64) to change in heifer BW and increased (P less than .01) as BW loss increased during gestation. After parturition, mean LH peak amplitude and area under the response curve averaged 50% less (P less than .10) in the BW loss and maintenance groups than in the BW gain group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Elicitation of release of luteinizing hormone by N-methyl-d,l-aspartic acid during three paradigms of suppressed secretion of luteinizing hormone in the female pig.

Two experiments were conducted to determine the minimal effective dose during lactation and site of action of N-methyl-d,l-aspartic acid (NMA) for elicitation of release of luteinizing hormone (LH) in female pigs. In the first experiment, three doses of NMA were given to lactating primiparous sows in which endogenous LH was suppressed by suckling of litters. In the second experiment, ovariectomized gilts were pretreated with estradiol benzoate or porcine antisera against GnRH to suppress LH and then given NMA to determine if it elicited secretion of LH directly at the anterior pituitary or through release of GnRH. In experiment 1, 3 lactating sows (17 +/- 1.5 d postpartum) were each given three doses of NMA (1.5, 3.0 and 5.0 mg/kg body weight [BW]; IV) on 3 consecutive days in a Latin Square design. Blood samples were collected every 10 min from -1 to 1 hr from injection of NMA. NMA at 1.5 and 3.0 mg/kg did not affect (p greater than .5) secretion of LH; however, 5 mg NMA/kg elicited a 114% increase (p less than .001) in circulating levels of LH during 1 hr after treatment. In experiment 2, 8 ovariectomized gilts were given either estradiol benzoate (EB; 10 micrograms/kg BW; IM n = 4) to suppress release of GnRH or porcine antiserum against GnRH (GnRH-Ab; titer 1:8,000; 1 ml/kg BW; IV; n = 4) to neutralize endogenous GnRH. Gilts infused with GnRH-Ab were given a second dose of antiserum 24 hr after the first. Gilts were then given NMA (10 mg/kg BW; IV) 33 hr after EB or initial GnRH-Ab. Blood samples were drawn every 6 hr from -12 to 24 hr from EB or GnRH-Ab treatments, and every 10 min from -2 to 2 hr from NMA. Serum LH declined (p less than .001) after EB (from 1.87 +/- .2 ng/ml at 12 hr before EB to 0.46 +/- .02 ng/ml during 24 hr after EB) and GnRH-Ab (from 1.97 +/- .1 to 0.59 +/- .02 ng/ml). In gilts treated with EB, the area under the curve (AUC) for the LH response (ng.ml-1.min) 1 hr after NMA (38.7 +/- 3) was significantly greater (p less than .01) than the 1 hr prior to NMA (21.3 +/- 1.5). Treatment with NMA had no effect (p greater than .5) on secretion of LH in gilts infused with GnRH-Ab.(ABSTRACT TRUNCATED AT 400 WORDS)     

Secretion of luteinizing hormone into pituitary venous effluent of the follicular and luteal phase mare: novel acceleration of episodic release during constant infusion of gonadotropin-releasing hormone

We tested the hypothesis that continuous infusion of native GnRH into mares during the estrous cycle, at a dose of 100 μg/h, would elevate circulating concentrations of LH without disrupting the endogenous, episodic pattern of LH release. Ten cyclic mares were assigned to one of two groups (n = 5/group): (1) Control (saline) and (2) GnRH in saline (100 μg/h). On experimental day 0 (3 to 6 d after ovulation), osmotic pumps containing saline or GnRH were placed subcutaneously and connected to a jugular infusion catheter. Blood samples were collected from jugular catheters daily and at 5-min intervals from catheters placed in the intercavernous sinus (ICS) for 8 h on experimental day 4 (luteal phase; 7 to 10 d after ovulation), followed by an additional 6-h intensive sampling period 36 h after PGF(2α)-induced luteal regression (experimental day 6; follicular phase). Treatment with GnRH increased (P < 0.001) concentrations of LH by 3- to 4-fold in the peripheral circulation and 4- to 5-fold in the ICS. Continuous GnRH treatment accelerated (P < 0.01) the frequency of LH release and decreased the interepisodic interval during both luteal and follicular phases. Treatment with GnRH during the luteal phase eliminated the low-frequency, long-duration pattern of episodic LH release and converted it to a high-frequency, short-duration pattern reminiscent of the follicular phase. These observations appear to be unique to the horse. Further studies that exploit this experimental model are likely to reveal novel mechanisms regulating the control of gonadotrope function in this species.     

Endogenous opioid suppression of release of luteinizing hormone during suckling in postpartum anestrous beef cows

Beef cows were used to determine if suckling influences release of LH via endogenous opioids at 28 +/- 4 d after parturition. Cows of similar weight and body condition (6.8 +/- .1, 1 = emaciated, 9 = obese) were assigned randomly to five groups (n = 6 to 7): 1) control-suckled/saline (suckled 15 min every 6 hr for 48 hr); 2) control-suckled/naloxone; 3) calf-removal/saline (calf removal for 52 hr); 4) calf-removal/naloxone; and 5) control-suckled/GnRH (Gonadotropin-Releasing Hormone). At 0 hr, saline was administered to all cows. This treatment was continued at 6 hr intervals for 24 hr. Either naloxone (0.5 mg/kg), GnRH (40 ng/kg) or saline was administered to cows in their respective groups every 6 hr during the ensuing 24-hr period in calf-removal groups, or immediately preceding each suckling episode in the control-suckled groups. Blood samples for analysis of luteinizing hormone (LH) were collected at 15-min intervals for 1 hr prior to and 3 hr after treatment at 0, 24, 36 and 48 hr. Cows were observed for estrus twice daily. All cows in the control-suckled/GnRH group released LH (P less than .05) in response to exogenous GnRH, indicating the presence of releasable quantities of the gonadotropin. Mean concentrations of LH were not effected (P greater than .05) by the control-suckled regime. However, calf-removal alone, or in combination with naloxone, increased (P less than .05) mean concentrations of LH by 48 hr.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gonadotropin releasing hormone-induced secretion of luteinizing hormone during the milk-ejection reflex in the postpartum beef cow

A study was conducted to determine the effect of the milk-ejection reflex on exogenous gonadotropin releasing hormone (GnRH)-induced release of luteinizing hormone (LH) after short-term calf removal. Twenty-four postpartum multiparous beef cows were assigned randomly to groups arranged in a 2(3) factorial arrangement. Factors consisted of two levels of suckling [suckled (S) or nonsuckled (NS)], treatment with GnRH [saline (C) or 200 micrograms GnRH] and days postpartum (d 1 and 14). Dams were isolated from their calves for 4 h on d 1 and 14 postpartum. At the end of 4 h dams were reunited with their calves in S + C and S + GnRH groups, while dams of calves in NS + C and NS + GnRH groups remained separated an additional 2 h. Cows were injected iv with saline or GnRH following the 4-h isolation period, 5 min after calves had begun suckling or nuzzling the udder. Sera from jugular blood samples collected 15 min prior to the end of the 4-h isolation period, immediately prior to injection (0 h) and at 15 min intervals thereafter for 120 min were analyzed for LH. Serum concentrations of LH in control cows did not differ due to suckling or stage of the postpartum period and averaged 2.3 +/- .1 ng/ml. Pituitary response to GnRH was determined by computing the rate of LH release. Rate of LH release (ng LH.ml-1.min-1) in response to GnRH on d 14 was greater (P less than .001) than on d 1 in both suckled and nonsuckled groups (S + GnRH, 37.1 +/- 3.9 vs 18.3 +/- 5.0; NS + GnRH, 34.7 +/- 5.9 vs 14.5 +/- 1.1). However, GnRH-induced release of LH did not differ between suckled and nonsuckled cows on either d 1 or 14 postpartum. These data indicate that response of the bovine pituitary to GnRH during the postpartum period is not influenced by the act of suckling but is enhanced with time after parturition.     

Effect of castration on plasma luteinizing hormone concentrations in prepubertal boars

Mean concentrations and the occurrence of pulsatile release of luteinizing hormone (LH) were determined in 14-wk-old crossbred boars (50.5 +/- 1.5 kg) after bilateral or unilateral castration at 10 wk of age. Blood was collected at 10-min intervals for 5 h. Then gonadotropin releasing hormone (GnRH; 40 micrograms) was given and sampling was continued at 5-min intervals for 1 h. Compared with intact boars, bilateral castration increased (P less than .001) mean LH (982 +/- 56 vs 389 +/- 56 pg/ml), pulsatile releases of LH (7.0 +/- .6 vs 2.0 +/- .6 pulses/5 h) and LH pulse amplitude (617 +/- 29 vs 360 +/- 58 pg/ml). Unilaterally castrated boars did not differ from intact boars in any of the above measures of LH secretion. Testis weight increased more between 10 and 14 wk of age in the unilateral castrates than in the intact boars (432 +/- 42 vs 245 +/- 34%; P less than .05). Thus, compensatory hypertrophy occurred within 4 wk of castration. Plasma testosterone was lower for bilateral castrates than for intact animals (.1 +/- .8 vs 3.6 +/- .9 ng/ml; P less than .05) while unilateral castrates (3.8 +/- 1.0 ng/ml) and intact boars did not differ. Plasma estradiol concentrations in bilateral and unilateral castrates were not different from levels found in intact boars (1.8 +/- 1.8, 8.8 +/- 2.1 and 6.0 +/- 1.8 pg/ml, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of nutritional level and biological type on gonadotropin-releasing hormone-induced luteinizing hormone release and plasma progesterone, estrone and estradiol concentrations in pre- and post-partum beef heifers

Forty-six beef heifers (16 to 23 mo) of two biological types (small = Red Poll-sired, large = Charolais-sired) were individually fed from d 90 of gestation through parturition to evaluate the effects of nutritional restriction on plasma LH and steroid hormone concentrations. Heifers were allotted to one of two nutritional treatments to achieve a BW reduction (loss, fed at 1% of BW/d) or to maintain initial BW (maintenance, fed 1.5% of BW/d) to parturition. Gonadotropin-releasing hormone (100 micrograms) was injected i.m. three times during gestation (d 130; d 200; d 270) and twice after parturition (d 1 to 14; d 23 to 36). Blood samples were collected at 20-min intervals after GnRH for 4 h. Maternal BW change from d 90 to parturition differed (P less than .01) between loss and maintenance heifers. Mean plasma progesterone concentrations were greater (P less than .05) at d 130 and 270 of gestation in small than in large heifers and were greater (P less than .01) at d 23 to 36 postpartum in maintenance than in loss heifers. Mean concentrations of estrone and estradiol were greater (P less than .05) in large than in small heifers at d 200 of gestation. Mean plasma LH concentrations following GnRH injection were greater (P less than .01) in loss than in maintenance heifers at 200 and 270 d of gestation. Metabolizable and retained energy were related inversely to LH release during mid and late gestation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postpartum reproduction in protein restricted beef cows: effect on the hypothalamic-pituitary-ovarian axis

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 less than .05) from 20 to 60 d in ADQ cows. Basal and mean LH were not affected (P greater than .10) by CP restriction or by days after parturition. Crude protein did not affect pituitary GnRH receptors (P greater than .10), but it did affect pituitary LH content, FSH content and FSH concentration (P less than .05). In Exp. 2, 28 cows were assigned to treatment groups as in Exp. 1. All cows were challenged with GnRH (.22 micrograms/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 less than .07). Deficient CP decreased GnRH-induced LH release (P less than .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-17 beta (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 greater than .10), whereas time to E2-induced LH peak decreased as time after parturition increased in ADQ cows (P less than .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.     

Steroid hormone and luteinizing hormone concentrations in the anestrous sow.

This investigation characterized serum concentrations of luteinizing hormone (LH), estradiol-17 beta (E2), progesterone (P4) and cortisol (C) in anestrous sows. Twenty-two sows that had not returned to estrus within 45 days after weaning (anestrous sows), and ten sows that had returned to estrus within seven days following weaning (cyclic sows) were nonsurgically fitted with indwelling jugular vein cannulae. Blood samples were collected at 6 h intervals for seven days and at 15 min intervals for 8 h on the fifth day after cannulation. Serum LH concentrations were determined in all samples, while C, E2 and P4 levels were quantitated in serum collected at 6 h intervals. Serum P4 concentrations in anestrous sows were consistently less than 0.5 ng/mL, and E2 levels ranged from 10 to 19 pg/mL. Concentrations of LH remained less than 1.0 ng/mL in anestrous sows, whereas a preovulatory LH surge was observed in five of ten cyclic sows. There was a circadian rhythm in mean C levels with C peaks occurring at 0600 or 2400 h and nadir levels observed at 1200 and 1800 h. Few differences in C levels were detected between anestrous and cyclic sows. It was evident that anestrous sows did not exhibit cyclic or predictable variations in steroid hormone concentrations. Unfortunately, the results of this study failed to elucidate the endocrine pathogenesis of the anestrous sow.     

Effects of season and stage of gestation on luteinizing hormone release in gilts.

This study was designed to examine the effects of two seasons and stage of gestation on luteinizing hormone (LH) release in the gilt. Eleven Yorkshire-Landrace crossbred gilts were each fitted with an indwelling vena caval cannula. Blood samples were collected at 6 h intervals for six days during early (day 39 to 44) or mid-gestation (day 69 to 74). Serum progesterone, estradiol-17 beta and LH concentrations were determined in samples collected at 6 h intervals. Early and mid-gestation occurred during August and September in group 1 (n = 6) and during January and February in group 2 gilts (n = 5). To characterize pulsatile LH release, samples were collected at 15 min intervals for 8 h on day 40, 43, 70 and 73 of gestation. Following each 8 h sampling period, gilts were treated intravenously with 0.5 micrograms gonadotropin-releasing hormone (GnRH)/kg body weight and blood collected at 10 min intervals for 3 h. Progesterone concentrations decreased (p less than 0.01) from 22.1 +/- 0.4 ng/mL during early gestation to 18.2 +/- 0.4 ng/mL during mid-gestation. Estradiol-17 beta concentrations increased (p less than 0.01) from early to mid-gestation (13.5 +/- 0.8 versus 28.4 +/- 0.7 pg/mL). Frequency of LH pulses and LH pulse amplitude were higher (p less than 0.05) in pregnant gilts during January and February compared to August and September.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of restriction of energy during lactation on body condition, energy metabolism, endocrine changes and reproductive performance in primiparous sows

Seventeen Landrace X Large White primiparous sows that farrowed in August 1982 were fed ad libitum (AL, n = 8) or their intakes were restricted (R, n = 9) during lactation. Litter sizes were equalized after farrowing and pigs were not allowed creep feed. Pigs were weaned 23.8 +/- .4 d postpartum. On d 6, 12 and 20 postpartum, all sows were fasted for 16 h and blood samples were collected prior to feeding for analysis of plasma glucose (GLU), urea nitrogen (UN), free fatty acids (FFA), prolactin (PRL) and serum insulin (INS). On d -2, 2 and 4 from weaning, sows were fasted for 16 h and then blood samples were collected hourly from 0 to 6 postprandial for analysis of GLU, UN, FFA, PRL and INS. Serum for analysis of luteinizing hormone (LH), progesterone and estradiol was collected every 6 h from 1 d before until 12 d after weaning. Samples for LH were also collected at 15-min intervals for 3 h at -18, -6, 6, 18, 78, 102, 126, 150, 240 and 480 h from weaning. After weaning all sows were fed 1.8 kg X d-1, and were checked for estrus twice daily. Daily intakes of metabolizable energy (ME) during lactation were greater in AL (12,194 +/- 465 kcal) than in R sows (8,144 +/- 90 kcal). Compared with AL sows, R sows lost more weight and backfat during lactation and had higher postprandial UN levels 2 d before and 4 d after weaning. Reproductive performance and reproductive hormones were not affected by restriction of energy, but frequency of episodic release of LH prior to weaning was greater in sows that exhibited estrus after weaning (n = 12) than in anestrous sows (n = 5). After weaning, LH and estradiol concentrations were similar between estrous and anestrous sows until onset of the preovulatory increase in estradiol in the sows that exhibited estrus. Energy intake, body condition and productivity were similar between anestrous sows and sows that exhibited estrus. On d 12 and 20 of lactation, preprandial levels of GLU were greater and FFA were lower in anestrous than estrous sows. We conclude that restriction of feed intake during lactation affected body condition and metabolism of primiparous sows, but reproductive performance and productivity were not affected. Aberrations in partitioning of energy during lactation may predispose primiparous sows to postweaning anestrus, but the mechanisms by which this occurs have yet to be defined.     

Ovulation and embryonic survival in pubertal gilts treated with gonadotropin releasing hormone

An experiment was conducted to evaluate the effect of exogenous gonadotropin releasing hormone (GnRH) on ovulation and embryonic survival in pubertal gilts. Gilts were assigned in replicates to a control (n = 10) and treatment (n = 10) group. Treatment consisted of an iv injection of 200 micrograms of GnRH immediately after initial mating on the first day of detected estrus. Control gilts were similarly injected with physiological saline. Blood samples were collected from the anterior vena cava immediately prior to injection, thereafter at 15-min intervals for 90 min, and subsequently, before slaughter on d 30 of gestation. Serum samples were analyzed for luteinizing hormone (LH) and progesterone by radioimmunoassay. Treatment with GnRH increased the quantity of LH released (P less than .05), with highest serum concentrations (ng/ml, means +/- SE) of gonadotropin in treated gilts (17.3 +/- 3.5) occurring at 75 min post-injection. In control gilts, serum concentrations of LH were not affected by injection of saline. Mean number of ovulations in treated gilts was also greater (P less than .05) than that of control animals (14.5 +/- .7 vs 12.1 +/- .6). However, treatment with GnRH did not enhance the number of attached conceptuses (normal and degenerating) present (treated, 10.9 +/- .9 vs control, 10.5 +/- .7) nor the percentage of viable fetuses (treated, 74.7 +/- 6.9 vs control, 83.5 +/- 5.0%) on d 30 of gestation. Although GnRH increased ovulation rate, mean weight of corpora lutea of treated and control gilts did not differ (402.8 +/- 16.3 vs 389.5 +/- 11.3 mg, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)     

Chronic administration of recombinant ovine leptin in growing beef heifers: effects on secretion of LH, metabolic hormones, and timing of puberty

Serum concentrations of leptin increase linearly from approximately 16 wk before until the week of pubertal ovulation in beef heifers. To test the hypothesis that exogenous leptin can hasten the onset of puberty in heifers, we examined the effects of chronic administration of recombinant ovine leptin (oleptin) on timing of puberty, pulsatile and GnRH-mediated release of LH, and plasma concentrations of GH, IGF-I, and insulin. Fourteen fall-born, prepubertal heifers (Brahman x Hereford, 12 to 13 mo; 304.7+/-4.12 kg) were used. Heifers were stratified by age and BW and assigned randomly to one of two groups (seven animals per group): 1) Control; heifers received s.c. injections of saline twice daily (0700 and 1900) for 40 d; and 2) Leptin; heifers received s.c. injections of oleptin (19.2 microg/kg) twice daily at 0700 and 1900 for 40 d. Blood samples were collected at 10-min intervals for 5 h on. d 0, 5, 10, 20, 30, and 40, and twice daily, just before each treatment injection, throughout the study. On d 41, heifers received i.v. injections of GnRH at 0 (0.0011 microg/kg) and 90 min (0.22 microg/kg), with additional sampling for 5.5 h to examine releasable pools of LH. Diets promoted a gain of 0.32+/-0.09 kg/d, which did not differ between groups. Plasma concentrations of leptin increased markedly in leptin-treated heifers and were greater (P < 0.001) than controls throughout (27.8+/-0.8 vs. 4.9+/-0.12 ng/mL). None of the heifers reached puberty during the experiment, but did so within 45 d of its termination. Mean concentrations of plasma LH, GH, IGF-I, and insulin were not affected by treatment, nor was there an overall effect on the frequency of LH pulses. However, a treatment x day interaction (P = 0.02) revealed that the frequency of LH pulses (pulses/ 5 h) was greater (P = 0.03) in controls (3.6+/-0.36) than in leptin-treated heifers (1.7+/- 0.28) on d 10. Characteristics of GnRH-induced release of LH were not affected by treatment. In summary, chronically administered leptin failed to induce puberty or alter endocrine characteristics in beef heifers nearing the time of expected puberty.     

Reproductive, metabolic, and endocrine responses to feed restriction and GnRH treatment in primiparous, lactating sows

The current experiment was carried out to determine whether exogenous GnRH treatment in primiparous, lactating sows undergoing feed restriction would improve reproductive performance after weaning. Sows were allocated to one of three treatments: AA sows (n = 8) were fed to appetite throughout a 28-d lactation, AR (n = 12) and AR + GnRH (n = 12) sows were fed as AA sows from farrowing to d 21 of lactation, and feed intake was reduced to 50% of the ad libitum intakes from d 22 to 28. The AR + GnRH sows received 800 ng of GnRH i.v. every 6 h from d 22 to 28 of lactation, and AA and AR sows received saline. Sow weight, backfat, and litter weight were recorded weekly. Within 2 d after farrowing, litter size was standardized to 8 to 10. At d 17 of lactation, an indwelling jugular catheter was surgically implanted in each sow. Blood samples were taken for characterization of plasma LH, FSH, insulin, IGF-I, and leptin by RIA at d 21 and before and after weaning on d 28 of lactation. After weaning, all sows were given ad libitum access to feed, checked for onset of standing estrus twice daily with mature vasectomized boars, and inseminated 12 and 24 h after onset of standing estrus with pooled semen from the same fertile boars (3 x 10(9) sperm/AI). After breeding, feed allowance was reduced to NRC (1988) requirements for gestation. At d 28 +/- 3 of gestation, sows were killed and ovulation rate and embryo survival were determined. Restricted sows lost more weight during lactation than AA sows (P < .02). During the period of feed restriction, plasma IGF-I and postprandial insulin and leptin in AR and AR + GnRH sows, and LH pulse frequency in AR sows, were lower than those in AA sows (P < .04). Associations (P < .004) between plasma insulin and leptin and between leptin and mean LH concentrations were established. The LH pulse frequency in AR + GnRH sows did not differ from that in AA sows before weaning. After weaning, maximum, mean, and minimum LH concentrations in the AA and AR sows, and FSH concentrations in AR sows, increased (P < .05) in response to weaning. Paradoxically, GnRH treatment in lactation seemed to suppress the expected LH and FSH responses to weaning. Ovulation rate and embryo survival were not different among the three groups. In conclusion, although exogenous GnRH therapy restored LH secretion in feed-restricted sows, it did not improve overall reproductive performance.     

Hourly administration of GnRH to prepubertal gilts: endocrine and ovulatory responses from 70 to 190 days of age.

This study investigated the responsiveness of the pituitary-ovarian axis of prepubertal gilts to hourly injections (i.v.) with GnRH. Six gilts each at 70, 100, 150, and 190 d of age were assigned either to treatment with GnRH or saline. Treatments were given until gilts showed estrus or for 7 d, whichever came first. Hourly pulsing with GnRH resulted in gradually increasing concentrations of estradiol-17 beta (E2), a preovulatory surge of LH, and subsequently increased progesterone (P4) concentrations. The increase in serum P4 was preceded by ovulation and corpora lutea (CL) formation in two gilts 70 d of age and all older gilts. The interval (h) from start of GnRH treatment to peak E2 (88 +/- 3), peak LH (103 +/- 3), and concentrations of P4 greater than or equal to 1 ng/mL (144 +/- 4) did not differ (P greater than .50) for 18 gilts between 100 and 190 d of age. In two ovulating, 70-d-old gilts, the interval from onset of GnRH treatment to peak E2 (171 +/- 6), peak LH (186 +/- 0), and P4 greater than or equal to 1 ng/mL (216 +/- 4) was lengthened (P less than .001). Peak concentrations of E2 (pg/mL) were higher (P less than .01) at 190 d (48 +/- 2) and 150 d (49 +/- 2) than at younger ages and lower (P less than .01) in gilts 70 d of age (31 +/- 1) than in gilts 100 d of age (41 +/- 2). Peak LH (nanograms/milliliter) was higher (P less than .01) in gilts 100 d of age (12.7 +/- 6) than in older gilts. Concentrations of P4 were similar (P greater than .20) for all ovulating gilts. The number of CL (12.7 +/- .7) did not differ (P greater than .20) for 18 gilts 100 d of age or older but was higher (P less than .01) than that (4.5 +/- 1.1) for two gilts 70 d of age. Corresponding endocrine responses or ovulations were not observed in four 70-d-old gilts treated with GnRH or in gilts given saline. These findings indicate that the functional integration of the pituitary-ovarian axis is completed between 70 and 100 d of age. Hourly treatment with GnRH is an adequate stimulus to induce ovulation in prepubertal gilts as early as 70 d of age. Also, the number of follicles reaching ovulatory competency was similar (P greater than .20) in gilts between 100 and 190 d of age, when GnRH was given on a BW basis.