Serum leptin concentrations, luteinizing hormone and growth hormone secretion during feed and metabolic fuel restriction in the prepuberal gilt

Two experiments were conducted to determine 1) the effect of acute feed deprivation on leptin secretion and 2) if the effect of metabolic fuel restriction on LH and GH secretion is associated with changes in serum leptin concentrations. Experiment (EXP) I, seven crossbred prepuberal gilts, 66 +/- 1 kg body weight (BW) and 130 d of age were used. All pigs were fed ad libitum. On the day of the EXP, feed was removed from four of the pigs at 0800 (time = 0) and pigs remained without feed for 28 hr. Blood samples were collected every 10 min from zero to 4 hr = Period (P) 1, 12 to 16 hr = P 2, and 24 to 28 hr = P 3 after feed removal. At hr 28 fasted animals were presented with feed and blood samples collected for an additional 2 hr = P 4. EXP II, gilts, averaging 140 d of age (n = 15) and which had been ovariectomized, were individually penned in an environmentally controlled building and exposed to a constant ambient temperature of 22 C and 12:12 hr light: dark photoperiod. Pigs were fed daily at 0700 hr. Gilts were randomly assigned to the following treatments: saline (S, n = 7), 100 (n = 4), or 300 (n = 4) mg/kg BW of 2-deoxy-D-glucose (2DG), a competitive inhibitor of glycolysis, in saline iv. Blood samples were collected every 15 min for 2 hr before and 5 hr after treatment. Blood samples from EXP I and II were assayed for LH, GH and leptin by RIA. Selected samples were quantified for glucose, insulin and free fatty acids (FFA). In EXP I, fasting reduced (P < 0.04) leptin pulse frequency by P 3. Plasma glucose concentrations were reduced (P < 0.02) throughout the fast compared to fed animals, where as serum insulin concentrations did not decrease (P < 0.02) until P 3. Serum FFA concentrations increased (P < 0.02) by P 2 and remained elevated. Subcutaneous back fat thickness was similar among pigs. Serum IGF-I concentration decreased (P < 0.01) by P 2 in fasted animals compared to fed animals and remained lower through periods 3 and 4. Serum LH and GH concentrations were not effected by fast. Realimentation resulted in a marked increase in serum glucose (P < 0.02), insulin (P < 0.02), serum GH (P < 0.01) concentrations and leptin pulse frequency (P < 0.01). EXP II treatment did not alter serum insulin levels but increased (P < 0.01) plasma glucose concentrations in the 300 mg 2DG group. Serum leptin concentrations were 4.0 +/- 0.1, 2.8 +/- 0.2, and 4.9 +/- 0.2 ng/ml for S, 100 and 300 mg 2DG pigs respectively, prior to treatment and remained unchanged following treatment. Serum IGF-I concentrations were not effected by treatment. The 300 mg dose of 2DG increased (P < 0.0001) mean GH concentrations (2.0 +/- 0.2 ng/ml) compared to S (0.8 +/- 0.2 ng/ml) and 100 mg 2DG (0.7 +/- 0.2 ng/ml). Frequency and amplitude of GH pulses were unaffected. However, number of LH pulses/5 hr were decreased (P < 0.01) by the 300 mg dose of 2DG (1.8 +/- 0.5) compared to S (4.0 +/- 0.4) and the 100 mg dose of 2DG (4.5 +/- 0.5). Mean serum LH concentrations and amplitude of LH pulses were unaffected. These results suggest that acute effects of energy deprivation on LH and GH secretion are independent of changes in serum leptin concentrations.     

Comparison of luteinizing hormone and steroid hormone secretion during the peri- and post-ovulatory periods in Mangalica and Landrace gilts

The objective of this study was to determine plasma concentrations of luteinizing hormone (LH), progesterone (P4) and estradiol-17beta (E2) in Mangalica gilts (M), a Hungarian native breed, and compare them with Landrace gilts (L) during the peri- and post-ovulatory periods. The estrous cycle of gilts was synchronised by Regumate feeding, and ovulation was induced with a gonadotropin-releasing hormone (GnRH) agonist. Blood sampling was carried out via indwelling jugular catheters three times a day and in 2-h intervals during a 16-h period after the GnRH application. The concentrations of LH, E2 and P4 were determined by immunoassays. Gilts of both breeds showed a typical gonadotropin and gonadal hormone secretion pattern. Preovulatory E2 peaks were observed on day 2 (M) and day 4 (L) after the last Regumate feeding. Highest E2 concentration was different between M and L breeds (46.5 +/- 5.7 vs. 26.0 +/- 6.8 pg/ml, P < 0.05). Maximum LH levels measured up to 6 h after GnRH were not different between M and L breeds (11.5 +/- 4.1 vs. 6.6 +/- 2.3 ng/ml). Both LH amounts during surge (41.1 +/- 15.9 vs. 27.5 +/- 6.1 ng/ml) and total over LH release (73.4 +/- 22.2 vs. 50.0 +/- 8.7 ng/ml) did not differ significantly between M and L breeds. P4 concentrations started to rise on day 6 after Regumate feeding and increased significantly from 0.6 +/- 0.3 and 0.7 +/- 0.4 ng/ml to maximal 14.0 +/- 2.4 and 11.3 +/- 2.1 ng/ml in M and L breeds, respectively. Mean P4 secretion was higher in M on days 10-15 (12.9 +/- 2.6 vs. 9.3 +/- 2.2 ng/ml; P<0.05). At the same time the number of corpora lutea was lower in M compared to L (10.3 +/-1.5 vs. 17.8 +/- 5.0, P<0.05). In our experiment, there was no evidence that differences in the secretion of analysed hormones during the peri- and post-ovulatory periods are a possible cause of usually lower fecundity in Mangalica gilts.     

Cortisol and luteinizing hormone after adrenocorticotropic hormone administration to postpartum beef cows

Cortisol and luteinizing hormone (LH) were measured in serum after the administration of adrenocorticotropic hormone (ACTH) to suckled (S) and nonsuckled (NS) beef cows. Blood was sampled on 2 consecutive days every 2 weeks for four bleeding periods starting 14 days after calving. Cows were injected with 200 IU ACTH or saline in a 2-day switchback design. Serum was collected before ACTH or saline injection and at 30-min intervals thereafter for 8 hours. Average cortisol concentrations in serum were similar in S and NS cows (6.4 +/- .6 and 6.1 +/- .8 ng/ml, respectively) after saline. Average cortisol concentrations in serum collected during an 8-hr period after ACTH on days 14, 28, 42 and 56 postpartum were 24.7 +/- 2.4, 31.8 +/- 3.5, 36.4 +/- 4.2 and 40.7 +/- .5 ng/ml, respectively, for S cows, and 31.1 +/- 2.9, 44.7 +/- 5.2, 45.0 +/- 5.7 and 46.0 +/- 5.4 ng/ml, respectively, for NS cows. Cortisol response to ACTH, measured as area under the response curve, was greater (P less than .05) in NS than in S cows. Amount of cortisol released by 200 IU ACTH was maximal by days 28 to 29 postpartum in NS cows, but the response increased gradually between days 14 to 15 and days 56 to 57 in S cows. overall, LH in serum averaged .55 +/- .08 ng/ml for S cows and .92 +/- .06 ng/ml for NS cows after saline, and .49 +/- .07 ng/ml for S cows and .94 +/- .06 ng/ml for NS cows after ACth. Although mean and peak serum LH concentrations did not differ between cows given ACTH and those given saline, the number of LH peaks and the number of cows having LH after saline. Mean serum LH concentrations were lower (P less than. 05) in S than in NS cows at 28 days postpartum. The number of LH peaks was lower (P less than .05) and the magnitude of the largest LH peak tended to be lower (P less than .06) in S cows at all sampling periods.     

Plasma concentrations of luteinizing hormone and adrenocorticotropic hormone in blood collected during the luteal and follicular phases of the estrous cycle in cows.

Luteinizing hormone (LH) and ACTH concentrations were measured in plasma from 7 cows to determine whether ACTH secretion changes with the phase of the estrous cycle, and to determine whether any ACTH peaks are associated with LH peaks. Blood was collected every 5 minutes for 190 minutes during the luteal and follicular phases of the estrous cycle. Radioimmunoassays were used to measure ACTH and LH in plasma. Mean concentration of ACTH in all cows did not differ significantly between luteal (35.1 +/- 8.0 pg/ml) and follicular (37.5 +/- 9.4 pg/ml) phases of the estrous cycle. Mean concentration of luteal-phase LH of all cows (2.0 +/- 1.1 ng/ml) was significantly (P less than 0.01) lower than mean concentration of follicular-phase LH (5.4 +/- 1.6 ng/ml). Frequency of peaks in ACTH concentration was low during the sampling period. Mean number of luteal-phase ACTH peaks (0.29 +/- 0.49) was not significantly different from that of follicular-phase samples (0.43 +/- 0.530). Unlike ACTH, mean frequency of LH peaks was significantly (P less than 0.05) higher in plasma from cows in the follicular phase of the estrous cycle (2.9 +/- 0.7), compared with that from cows in the luteal phase (0.29 +/- 0.49).     

Opioid control of growth hormone in the suckled sow is primarily mediated through growth hormone releasing factor

Endogenous opioid peptides mediate the effect of suckling on LH and PRL in the domestic pig. However, the role of opioids in modulating GH during lactation in swine is not known. Primiparous sows that had been immunized against GRF(1-29) conjugated to human serum albumin (GRF-HSA, n = 5) or HSA (n = 4) were used to determine changes in GH after naloxone. Treatments were imposed in all sows on day 21 of lactation when antibody titers were 9100 +/- 1629. All sows received (i.v.) naloxone (0.25 mg/kg) or saline (0.0125 ml/kg) at 15 min intervals for 165 min. Active immunization against GRF-HSA during lactation decreased (P less than 0.05) mean concentration (4.8 +/- 0.2 vs 2.6 +/- 0.1 ng/ml) and frequency (1.5 +/- 0.3 vs 0.4 +/- 0.2 peaks/4 hr). Concentrations of LH and PRL were similar in GRF-HSA and HSA immunized sows. Naloxone suppressed (P less than 0.05) GH in all sows. In HSA sows, naloxone abolished episodic release of GH and decreased average, but not basal, concentrations of GH. In sows immunized against GRF-HSA, naloxone decreased (P less than 0.05) average and basal GH but failed to decrease frequency of GH release. Naloxone failed to alter frequency of LH release. Concentrations of PRL decreased (P less than 0.05) after naloxone in all sows. In conclusion, immunization against GRF-HSA blocked most of the effect of lactation on GH. Blocking opioid receptors with naloxone decreased GH and PRL in all sows. In contrast to previous findings naloxone had no effect on LH. Opioids alter concentrations of GH through a GRF dependent and GRF independent pathway.     

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)     

Influence of the ovary and suckling on luteinizing hormone response to naloxone in postpartum beef cows

The influence of the suckling stimulus and ovarian secretions on LH response to naloxone was studied in 16 postpartum anestrous beef cows that were assigned randomly to one of four groups (n = 4/group): intact suckled (IS), intact nonsuckled (IN), ovariectomized suckled (OS) or ovariectomized nonsuckled (ON). Ovariectomy (OS + ON) and calf removal (IN + ON) were performed on d 2, 3 or 4 after parturition. Jugular venous blood was collected at 15-min intervals for 4 h before and 4 h after administration of naloxone (1 mg/kg BW, i.v.) on d 14 and d 28 after parturition. Gonadotropin-releasing hormone (5 micrograms, i.v.) was given 3 h after naloxone. Both IN and OS increased (P less than .05) mean pretreatment LH above IS values (mean +/- SE, ng/ml; IS 1.6 +/- .1 vs IN 2.5 +/- .3 and OS 2.7 +/- .4; P less than .01), whereas ON increased (P less than .01) LH (3.7 +/- .3 ng/ml) even further. Mean LH increased (P less than .05) after naloxone administration in all treatment groups. However, magnitude of this response was variable and dependent on ovarian status. Amplitude of the naloxone-induced LH response was greater (P less than .05) for ovariectomized (5.9 +/- 1.1 ng/ml) than for intact groups (2.7 +/- .5 ng/ml). Gonadotropin-releasing hormone increased mean LH concentrations in all groups. We suggest that ovarian secretions and the suckling stimulus contribute to endogenous opioid inhibition of LH during the postpartum interval.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of luteinizing hormone, leptin and progesterone levels in the systemic circulation (Vena jugularis) and near the ovarian circulation (Vena cava caudalis) during the oestrous cycle in Mangalica and Landrace gilts

The objective of this study was to evaluate luteinizing hormone (LH) and luteal progesterone (P4) secretion in systemic blood and blood near the ovaries in Mangalica (M) and Landrace (L) gilts by implanting catheters into the Vena jugularis and the Vena cava caudalis via the Vena saphena, respectively. Furthermore, leptin was analyzed in jugular vein blood. Blood was collected twice daily from day 7 to day 19 of the oestrous cycle and frequently (10-min intervals for 6 h) on day 9, day 12 and day 15 in M (n=3) and L gilts (n=4). L gilts had congruent pulsatile LH secretion in both veins, but the LH concentrations in M were always below the assay sensitivity during the luteal phase. In both breeds, episodic P4 secretion was found in the jugular and caval veins, and both sampling site and breed had an influence on P4 secretion (P<0.05). The mean concentration of P4 was higher (P<0.01) in utero-ovarian blood (75.8+/-5.3 in M; 49.6+/-4.2 ng/ml in L) than in the periphery (31.3+/-2.0 in M; 21.2+/-1.8 ng/ml in L). M pigs had a lower number of corpora lutea (9.7+/-2.3 vs. 20.5+/-4.4), and analysis of the P4 secretion ratio per corpus luteum revealed an influence of breed (P<0.01). This ratio was significantly higher in M (3.8+/-0.3 and 8.7+/-0.7 ng/ml) compared with the L gilts (1.4+/-0.1 and 2.8+/-0.3 ng/ml) in the jugular and caval veins, respectively. Blood sampling from the Vena cava caudalis is potentially more precise than from the Vena jugularis for evaluation of ovarian P4 secretion. Both the higher P4 concentration and increased leptin secretion (11.3+/-0.6 vs. 3.0+/-0.1 ng/ml, P<0.05) and consequently the altered LH secretion pattern in the Mangalica may contribute to the lower fecundity of this breed.     

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.     

Influence of calf removal on the serum luteinizing hormone response to naloxone in the postpartum beef cow

Twelve anestrous, postpartum beef cows were used to determine the effect of calf removal on the effect of naloxone on serum luteinizing hormone (LH) concentrations. On d 1, six cows were injected iv with saline and six with 200 mg naloxone dissolved in saline. Blood samples were taken at 15-min intervals for 2 h before and 2 h after naloxone or saline administration. At the beginning of blood sampling, calves were removed from three cows in each treatment. At 48 h after calf removal (d 3), all cows were injected iv with 200 mg naloxone and blood samples were collected as on d 1. On d 1, naloxone treatment increased (P less than .01) serum LH concentrations from 1.2 +/- .3 ng/ml at time 0 to 4.3 +/- .6 ng/ml and 4.7 +/- .8 ng/ml at 15 and 30 min, respectively. Injection of saline had no effect on serum LH concentrations. Forty-eight-hour calf removal increased (P less than .01) serum LH concentrations in five of six cows (1.7 +/- .8 vs 4.4 +/- 1.2 ng/ml). Naloxone treatment failed to increase serum LH concentrations in these cows. Injection of naloxone increased (P less than .01) serum LH concentrations in the one cow that did not exhibit an LH increase after calf removal and in six cows whose calves were not removed (1.4 +/- .2 vs 4.4 +/- .5 ng/ml). The present study provides additional evidence that endogenous opioids regulate LH in the postpartum beef cow. We hypothesize that suckling stimulates an opioid inhibition of LH secretion and removal of the suckling stimulus removes the opioid inhibitory tone.     

Luteinizing hormone release after administration of the gonadotropin-releasing hormone agonist Fertilan (goserelin) for synchronization of ovulation in pigs

The generic GnRH agonist, Fertilan (goserelin), was tested for the ability to induce an LH surge and ovulation in estrus-synchronized gilts. Three experiments were performed to 1) examine the effect of various doses of Fertilan on secretion of LH in barrows, to select doses to investigate in gilts (Exp. 1); 2) determine doses of Fertilan that would induce a preovulatory-like rise of LH in gilts (Exp. 2); and 3) determine the time of ovulation after Fertilan treatment (Exp. 3). In Exp. 1, 10 barrows were injected on d 1, 4, 7, 10, and 13 with 10, 20, or 40 microg of Fertilan; 50 microg of Gonavet (depherelin; GnRH control) or saline (negative control); and sequential blood samples were collected for 480 min. There was a dose-dependent stimulation (P < 0.05) of LH release. Maximal plasma concentrations of LH (LH(MAX)) were 2.1 +/- 0.2, 4.1 +/- 0.3, 2.6 +/- 0.4, and 3.4 +/- 0.3 ng/mL after 10, 20, and 40 microg of Fertilan and 50 microg of Gonavet, respectively, and duration of release was 78 +/- 9, 177 +/- 12, 138 +/- 7, and 180 +/- 11 min, respectively. Fertilan doses of 10 and 20 microg were deemed to be the most suitable for testing in gilts. In Exp. 2, 12 gilts received (after estrus synchronization with Regumate and eCG) injections of 10 or 20 microg of Fertilan or 50 microg of Gonavet 80 h after eCG to stimulate a preovulatory-like LH surge and ovulation. An LH surge was induced in 3 of the 4 gilts in both of the Fertilan groups and in all of the Gonavet-treated gilts. Characteristics of induced release of LH did not differ among groups: LH(MAX), 5.0 +/- 0.9 vs. 4.6 +/- 1.8 vs. 6.6 +/- 1.1 ng/mL; duration, 11.7 +/- 2.0 vs. 12.3 +/- 2.2 vs. 14.3 +/- 0.5 h; interval from GnRH injection to LH(MAX), 4.0 +/- 2.0 vs. 6.7 +/- 1.3 vs. 5.8 +/- 1.6 h. In Exp. 3, estrus-synchronized gilts were injected with 20 microg of Fertilan (n = 8) or 50 microg of Gonavet (n = 4), and the time of ovulation was determined by repeated endoscopic examination. Time of ovulation ranged from 34 to 42 h postGnRH; however, ovulation occurred earlier in the Gonavet compared with the other groups (P < 0.05). Results of these experiments indicate that 1) barrows are an appropriate model for determining GnRH doses that can be effective in inducing a preovulatory-like LH surge in females; 2) the generic GnRH agonist Fertilan, at doses of 10 to 20 microg, can stimulate an LH surge in gilts, with subsequent ovulation; and 3) Fertilan at doses of 10 and 20 microg should be examined further for use in fixed-time insemination protocols.     

Changes in serum concentrations of luteinizing hormone and follicle-stimulating hormone following injection of gonadotropin-releasing hormone during pregnancy and after parturition in mares

High concentrations of estrogens in the peripheral circulation during late gestation inhibit synthesis of LH and markedly reduce pituitary content of LH at the end of pregnancy in most domestic species. Because blood concentrations of estrogen peak shortly before mid-gestation in the mare and then gradually decrease until parturition, we hypothesized that pituitary content of LH may increase during late gestation. To test this hypothesis 10 horse mares were challenged with a maximally stimulatory dose (2 micrograms/kg) of GnRH on d 240 and 320 of gestation and d 3 after parturition. A separate group of four mares were treated with GnRH on d 2 or 3 estrus. Blood samples were collected at -2, -1, 0, .25, .5, .75, 1, 1.5, 2, 2.5, 3, 3.5, 4, 5, 6, 7 and 8 h relative to injection of GnRH and serum was analyzed for concentration of LH and FSH. Basal serum concentration and total quantity of LH released after GnRH stimulation (assessed by determining the area under the response curve) were not different on d 240 and 320 of gestation or on d 3 after parturition (12.5 +/- 3.5, 5.7 +/- 1.5 and 29.1 +/- 12.1 ng.min/ml, respectively) and were less (P less than .05) than on d 3 of estrus (311.0 +/- 54.0 ng.min/ml). There was little difference in the basal serum concentration of FSH at any of the time points examined. In contrast, GnRH-induced release of FSH continually decreased (P less than .05) from d 240 of gestation (559.8 +/- 88.9 ng.min/ml) to d 3 of estrus (51.8 +/- 6.2 ng.min/ml).(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Peri-oestrus hormone profiles and follicle growth in lactating sows with oestrus induced by intermittent suckling.

This study describes follicle dynamics, endocrine profiles in multiparous sows with lactational oestrus compared with conventionally weaned sows (C). Lactational oestrus was induced by Intermittent Suckling (IS) with separation of sows and piglets for either 12 consecutive hours per day (IS12, n = 14) or twice per day for 6 h per occasion (IS6, n = 13) from day 14 of lactation onwards. Control sows (n = 23) were weaned at day 21 of lactation. Pre-ovulatory follicles (> or =6 mm) were observed in 100% of IS12, 92% of IS6 and 26% of C sows before day 21 of lactation and in the remaining 74% C sows within 7 days after weaning. All sows with pre-ovulatory follicles showed oestrus, but not all sows showed ovulation. Four IS6 sows and one IS12 sow developed cystic follicles of which two IS6 sows partially ovulated. Follicle growth, ovulation rate and time of ovulation were similar. E(2) levels tended to be higher in IS sows (p = 0.06), the pre-ovulatory LH surge tended to be lower in IS12 (5.1 +/- 1.7 ng/ml) than in C sows (8.4 +/- 5.0 ng/ml; p = 0.08) and P(4) levels were lower in IS12 and IS6 than in C sows (at 75 h after ovulation: 8.8 +/- 2.4 ng/ml vs 7.0 +/- 1.4 ng/ml vs 17.1 +/- 4.4 ng/ml; p < 0.01). In conclusion, sows with lactational oestrus induced by IS are similar to weaned sows in the timing of oestrus, early follicle development and ovulation rates, but the pre-ovulatory LH surge and post-ovulatory P(4) increase are lower.     

Nutritionally induced relationships between insulin levels during the weaning-to-ovulation interval and reproductive characteristics in multiparous sows: I. Luteinizing hormone, follicle development, oestrus and ovulation

To get more insight in how insulin secretion patterns and corresponding insulin-like growth factor-1 (IGF-1) levels are related to luteinizing hormone (LH) secretion, follicle development and ovulation, 32 multiparous sows were fed either a dextrose plus lactose-containing diet at 4 h intervals (DL; each 150 g/day) or an isocaloric control diet at 12 h intervals (CTRL; containing soybean oil) during the weaning-to-ovulation interval (WOI). Insulin parameters (basal, peak levels and mean insulin) and IGF-1 levels during the WOI were similar for both treatments, but the insulin secretion pattern differed (related with feeding frequency and meal sizes). Oestrus and ovulation characteristics were not influenced by treatment. The LH surge was higher in CTRL compared with DL sows (3.73 vs 3.00 ng/ml; p = 0.03). Average diameter (6.5 vs 6.1 mm; p = 0.08) and uniformity (CV: 11 vs 15%, p = 0.02) of follicles ≥3 mm at day 4 after weaning was higher in CTRL compared with DL sows. Basal insulin levels were positively related with follicle diameter at ovulation (β = 0.05 mm/(μU/ml); p = 0.04) and negatively related with LH surge level (β = -0.07 (ng/ml)/(μU/ml); p = 0.01). Insulin area under the curve (AUC) (β = 0.037 (ng/ml)/1000 μU; p = 0.02) and IGF-1 levels (β = 0.002 (ng/ml)/(ng/ml); p < 0.01) were positively related to basal LH level around the LH surge. From these data, we conclude that insulin and IGF-1 levels during the WOI are related to LH secretion and follicle development. Not only the absolute level of insulin seems important, but also the pattern within a day in which insulin is secreted seems to affect LH secretion and development of pre-ovulatory follicles.     

Plasma cortisol and progesterone responses to low doses of adrenocorticotropic hormone in ovariectmized lactating cows

The objective of this study was to describe the responses of the plasma progesterone and cortisol concentrations in ovariectomized lactating cows to low doses of adrenocorticotropic hormone (ACTH). The estrous cycles in 3 lactating cows were synchronized, and the cows were ovariectomized in the luteal phase. ACTH challenge tests were conducted at doses of 3, 6, 12 and 25 IU. Blood samples were collected at 30 min intervals, and the plasma progesterone and cortisol concentrations were analyzed by EIA. A concomitant rise in plasma progesterone and plasma cortisol was observed in cows treated with 12 IU or higher doses of ACTH. Significant increments in the plasma cortisol concentrations were observed at all doses of ACTH. The means (+/- SE) of the peak plasma progesterone concentrations after the 3, 6, 12 and 25 IU ACTH challenge tests were 0.6 +/- 0.1, 1.3 +/- 0.4, 1.5 +/- 0.3 and 2.4 +/- 0.3 ng/ml, respectively. The means of the peak plasma cortisol concentrations in the 3 cows after the ACTH challenge were 14.0 +/- 1.5, 17.0 +/- 2.5, 23.3 +/- 3.0, and 33.3 +/- 7.0 ng/ml, respectively. The effects of the doses, time after treatment, and their interaction on the plasma progesterone concentrations after the ACTH challenge were significant (P<0.01). Likewise, the effects of the doses, time after treatment, and their interaction on the plasma cortisol concentrations after the ACTH challenge were significant (P<0.01). The mean AUC values for the plasma progesterone and cortisol concentrations after the ACTH treatments were also significantly affected by the dose of ACTH (P<0.01 and P<0.05, respectively). A significantly positive correlation was obtained between the peak plasma progesterone and cortisol concentrations after different doses of ACTH (r=0.7, P<0.05). The results suggest that lactating dairy cows are capable of secreting a significant amount of adrenal progesterone, reaching up to the minimal concentration necessary to cause suppression of estrus in response to 12 IU ACTH (P<0.01). The concomitant plasma cortisol concentration was 23.3 ng/ml.     

Effect of naloxone on serum luteinizing hormone, cortisol and prolactin concentrations in anestrous beef cows

Two experiments were conducted with the opioid antagonist naloxone to determine the effect of opioid receptor blockade on hormone secretion in postpartum beef cows. In Exp. 1, nine anestrous postpartum beef cows were used to measure the effect of naloxone on serum luteinizing hormone (LH), cortisol and prolactin concentrations. Cows received either saline (n = 4) or 200 mg naloxone in saline (n = 5) iv. Blood samples were collected at 15-min intervals for 2 h before and after naloxone administration. Serum LH concentrations increased (P less than .01) in naloxone-treated cows from 1.8 +/- .04 ng/ml before treatment to 3.9 +/- .7 ng/ml and 4.2 +/- .5 ng/ml at 15 and 30 min, respectively, after naloxone administration. In contrast, LH remained unchanged in saline-treated cows (1.6 +/- .3 ng/ml). Serum cortisol and prolactin concentrations were not different between groups. In Exp. 2, 12 anestrous postpartum beef cows were used to examine the influence of days postpartum on the serum LH response to naloxone. Four cows each at 14 +/- 1.2, 28 +/- .3 and 42 +/- 1.5 d postpartum received 200 mg of naloxone in saline iv. Blood samples were taken as in the previous experiment. A second dose of naloxone was administered 2 h after the first, and blood samples were collected for a further 2 h. Serum LH concentrations increased (P less than .01) only in cows at 42 d postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of short-term nutritional stimulus before and after the luteolysis on metabolic status, reproductive hormones and ovarian activity in goats

The effect of short-term nutritional supplementation on hormonal and ovarian dynamics was studied in goats. Cycling Shiba goats were divided randomly into maintenance (group M, n=4) and high-energy (group H, n=4) groups. After the detection of the ovulation (Day 0, 1(st) ovulation), group H received a high-energy diet providing 2.5 times of the maintenance energy requirement for 7 days from Day 7 to Day 13 and were administered 2 mg of prostaglandin F(2alpha) (PGF(2alpha)) on Day 10 to induce luteal regression followed by the follicular phase. Follicular and luteal dynamics were monitored using ultrasonography daily or every other day, and blood samples were collected daily from Day 0 to the third ovulation (3(rd) ovulation) following the second ovulation (2(nd) ovulation) induced by PGF(2alpha) administration. Blood samples were also collected at 10-min intervals for 6 h on Day 9 and Day 11 for analysis of pulsatile LH secretion. The mean concentrations of glucose and insulin were significantly (P<0.05) higher in group H than in group M on Days 8, 9, 12, 13 and Days 8, 9 and 10, respectively. For both the 2(nd) and 3(rd) ovulations, no significant difference was detected in ovulation rate between groups M and H. On the other hand, the interpeak interval for wave-like patterns of FSH in group H was significantly (P<0.05) shorter than in group M during the period between the 1(st) and 2(nd) ovulations (4.3 +/- 0.3 vs. 6.5 +/- 1.5 days). The mean LH pulse frequency in group H was significantly (P<0.05) greater than in group M on Day 11 (4.5 +/- 0.6 vs. 3.3 +/- 0.5 pulses/6 h). The present study clearly demonstrated that short-term (7 days) nutritional supplementation promoted pulsatile LH and wave-like FSH secretions in cycling goats. However, no significant increase in ovarian performance was found under such endocrine and metabolic conditions.     

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)     

Reduced postpartum anestrus of suckled beef cows treated with microencapsulated luteinizing hormone-releasing hormone analog.

This study evaluated the effect of microencapsulated LHRH agonist (D-Trp6-LHRH) on gonadotropin release and occurrence of estrus in early postpartum beef cows. Angus cows (n = 54) were assigned randomly to two treatment groups at d 5 postpartum. Group 1 received a single i.m. injection of D-Trp6-LHRH (LHRH-A) encapsulated in poly-DL-lactide-coglycolide, calculated to release 15 micrograms of LHRH-A per day for 30 d (n = 23). Group 2 received vehicle only (control, n = 31). Blood samples (15-min intervals for 6 h) were obtained on d 5, 10, 20, 30, and 40 postpartum for evaluation of LH and FSH concentrations (n = 12 per group). Days to first postpartum estrus were reduced by treatment with LHRH-A (Group 1, 43.7 +/- 4.2 d vs Group 2, 55.9 +/- 4.7 d; P < .05). However, days to conception were similar between groups (68.9 +/- 7.9 vs 76.7 +/- 6.7 d, respectively). On the day of treatment, cows treated with LHRH-A had higher mean concentrations of LH and FSH than did controls (8.3 +/- 1.4 vs 2.0 +/- .4 ng/mL for LH and 211.0 +/- 8.6 vs 51.2 +/- 2.7 ng/mL for FSH (P < .05). There were no differences in mean concentrations of LH or FSH between treatment groups on d 10, 20, 30, and 40 postpartum. Cows given LHRH-A had more (P < .05) LH pulses on d 10 and 30 postpartum than did controls. This study demonstrated that microencapsulated D-Trp6-LHRH reduced the postpartum anestrous interval in suckled beef cows.