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Biomedical subjects

M J Estienne

Publications and source records attributed to M J Estienne.

At least 37 records · Page 2Linked to original sources

Prolactin secretion after bromocriptine in the hypophysial stalk-transfected gilt.

Blood samples were collected by jugular vein cannula from 6 hypophysial stalk-transected (HST) and 4 intact (INTACT) crossbred gilts at 0800, 0830 and 0900 h. Immediately after the 0900 h sample, thyrotropin releasing hormone (TRH) was injected i.v. to determine anterior pituitary gland response via release of prolactin (PRL). Blood was collected every 15 min for 1 h and every 30 min for an additional 2 h. All gilts received the dopamine (DA) agonist, bromocriptine (CB-154), s.c. at 1600 h and blood sampling and TRH challenge was repeated beginning at 0800 h the next day. Mean serum PRL concentration at 0800, 0830 and 0900 h was termed basal PRL for each day. Before CB-154, basal PRL for HST gilts was greater (P < .01) than for INTACT gilts, whereas, after CB-154, basal PRL were similar among HST and INTACT gilts. Before CB-154, TRH caused peak secretion of PRL of similar magnitude within 15 minutes in both HST and INTACT gilts; PRL decreased to basal concentration by 120 min after TRH in both groups. However, after CB-154, PRL response to TRH was blunted similarly in all gilts. These results indicate that suppression of DA pathways is an antecedent to the physiological mechanism by which a secretagogue, such as TRH, stimulates PRL secretion in the intact pig.

Animals↗

Effects of intracerebroventricular administration of D,L-2-amino-5-phosphonovaleric acid, an N-methyl-D-aspartate receptor antagonist, on luteininizing hormone release in ovariectomized lambs.

To determine whether endogenous glutamate and aspartate control LH secretion via N-methyl-D-aspartate (NMDA) receptors in the sheep, we evaluated the effects of the NMDA receptor antagonist D,L-2-amino-5-phosphonovaleric acid (AP5) on secretion of LH in ovariectomized lambs. Twelve lambs were ovariectomized and surgically implanted with lateral cerebroventricular cannulae. At the time of the experiment, (38 wk of age) they received intracerebrally 4 injections of either 50 (n = 4), 100 (n = 4), or 200 micrograms (n = 4) of AP5. Blood samples were collected every 10 min for 8 h with animals receiving AP5 at hours 4, 5, 6, and 7. Patterns of LH during the preinjection period were compared to those during the period encompassing AP5 injections. Mean concentrations of LH were lower during AP5 injections than during the preinjection periods, a response that was not influenced by dose (0.87 +/- 0.08 vs. 0.69 +/- .07 ng/ml; p < 0.01). LH pulse amplitude decreased during AP5 treatment relative to the preinjection periods, but this difference was not statistically significant (0.79 +/- 0.11 vs. 0.68 +/- 0.10 ng/ml; p = 0.09). There were no effects of AP5 on LH pulse frequency (1.00 +/- 0.10 vs. 0.83 +/- 0.15 pulses/h for injection and preinjection periods; p > 0.10). A second experiment was done to evaluate a higher dose of AP5. Four animals were chosen to receive 4 injections of 2 mg of AP5 in a design identical to that used in the first experiment.

2-Amino-5-phosphonovalerate↗

Regression of induced corpora lutea in mature cyclic gilts by human chorionic gonadotropin.

This study was conducted to determine whether chronic hCG treatment would cause regression of induced corpora lutea (CL) in mature cyclic gilts. Thirty-two mature gilts that had displayed one or more estrous cycles of 18 to 22 d were used. Sixteen gilts were hysterectomized (HYSTX) on d 6 to 9 (d 0 = onset of estrus) and their CL were marked with charcoal (spontaneous group). Sixteen gilts (induced group) were injected with 1,500 IU of pregnant mare's serum gonadotropin (PMSG) on d 6 and 500 IU of hCG on d 9 (day of hCG = d 0 of the induced cycle). Ovulation was assumed to occur on d 2 of the induced cycle. Induced gilts were HYSTX on d 8 to 9 (d 17 to 18 of the original spontaneous cycle) and their CL were marked with charcoal. Only gilts (n = 14) in which induced CL were present and in which the original CL had regressed were then subjected to treatment with saline or hCG. From d 10 to 29, gilts with spontaneous CL were injected daily with 500 IU of hCG (n = 8) or saline (n = 8). From d 10 to 29 of the induced cycle, induced gilts were injected daily with 500 IU of hCG (n = 6) or saline (n = 8). Jugular blood samples were collected every other day from all gilts beginning on the 1st d of daily hCG treatment and quantified for estradiol and progesterone by RIA. On the day after the last hCG injection, the number of charcoal-marked CL and charcoal-marked corpora albicantia (CA) were determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Luteinizing hormone secretion in hypophysial stalk-transected gilts given hydrocortisone acetate and pulsatile gonadotropin-releasing hormone.

The site within the hypothalamic-pituitary axis at which cortisol acts to inhibit luteinizing hormone (LH) secretion was investigated in female pigs. Six ovariectomized, hypophysial stalk-transected (HST) gilts were given 1 microgram pulses of gonadotropin releasing-hormone (GnRH) iv every 45 min from day 0 to 12. On days 6-12, each of 3 gilts received either hydrocortisone acetate (HCA; 3.2 mg/kg body weight) or oil vehicle im at 12-hr intervals. Four ovariectomized, pituitary stalk-intact gilts served as controls and received HCA and pulses of 3.5% sodium citrate. Jugular blood was sampled daily and every 15 min for 5 hr on days 5 and 12. Treatment with HCA decreased serum LH concentrations and LH pulse frequency in stalk-intact animals. In contrast, serum LH concentrations, as well as the frequency and amplitude of LH pulses, were unaffected by HCA in HST gilts and were similar to those observed in oil-treated HST gilts. We suggest that chronically elevated concentrations of circulating cortisol inhibit LH secretion in pigs by acting at the level of the hypothalamus.

Animals↗

Endocrine changes in sows exposed to elevated ambient temperature during lactation.

Seven sows were placed into one of two environmental chambers at 22 C, 5 d prior to farrowing. On day 9 of lactation, one chamber was changed to 30 C (n = 4) and the other remained at 22 C (n = 3). On days 24 and 25, blood samples were collected every 15 min for 9 hr and 7 hr, respectively. On day 24, thyrotropin releasing hormone (TRH) and gonadotropin releasing hormone (GnRH) were injected iv at hour 8. On day 25 naloxone (NAL) was administered iv at hour 4 followed 2 hr later by iv injection of TRH and GnRH. Milk yield and litter weights were similar but backfat thickness (BF) was greater in 22 C sows (P less than .05) compared to 30 C sows. Luteinizing hormone (LH) pulse frequency was greater (P less than .003) and LH pulse amplitude was less (P less than .03) in 22 C sows. LH concentrations after GnRH were similar on day 24 but on day 25, LH concentrations after GnRH were greater (P less than .05) for 30 C sows. Prolactin (PRL) concentrations were similar on days 24 and 25 for both groups. However, PRL response to TRH was greater (P less than .05) on both days 24 and 25 in 30 C sows. Growth hormone (GH) concentrations, and the GH response to TRH, were greater (P less than .0001) in 30 C sows. Cortisol concentrations, and the response to NAL, were less (P less than .03) in 30 C sows. NAL failed to alter LH secretion but decreased (P less than .05) PRL secretion in both groups of sows. However, GH response to NAL was greater (P less than .05) in 30 C sows. Therefore, sows exposed to elevated ambient temperature during lactation exhibited altered endocrine function.

Animals↗

Physiological and nutritional responses of beef steers exposed to stable flies (Diptera: Muscidae).

Physiological and nutritional responses were measured in beef steers exposed to laboratory infestations of stable flies, Stomoxys calcitrans (L.). Calves (n = 6 per treatment) were infested with four levels of stable flies for three periods daily (15 min each period) for 14 d. Steers exposed to 0, 10, 20, or 30 stable flies consumed similar amounts of feed and water; they excreted similar amounts of feces and urine throughout the study. During the experiment, changes in body weight were not influenced by treatment. Heart and respiration rates, rectal temperatures, and circulating cortisol concentrations were similar among groups. Finally, nitrogen consumed, nitrogen lost in feces and urine, and nitrogen retained were unaffected by treatment. We suggest that intermittent exposure to these levels of stable flies, under the conditions of this study, does not evoke physiological and nutritional responses in beef steers.

Animal Nutritional Physiological Phenomena↗

Follicle growth in hypophysial stalk-transected pigs given pulsatile GnRH and pregnant mare serum gonadotropin.

In experiment 1, nine prepuberal crossbred gilts 145 +/- 2 days of age and 90.3 +/- 1.6 kg body weight (BW) were hypophysial stalk-transected (HST) or sham-HST. Starting at 0800 on Day 1 (35 +/- 2 days after surgery), three sham-HST and two HST gilts received 3.5% sodium citrate vehicle (V) while two HST gilts and two sham-HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 9 days via a jugular vein cannula. At 0800 on day 7, all gilts received 1,000 IU of pregnant mare serum gonadotropin (PMSG) im. Blood was sampled every 15 min from 0800 to 0845 on Days 1 through 6. On Day 10, ovarian morphology and ovarian and follicular fluid weights were recorded. In experiment 2, eight prepuberal crossbred gilts, 146 +/- 6 days of age and 79.5 +/- 1.5 kg BW, were HST or sham-HST. Starting at 0800 on Day 1 (7 +/- 4 days after surgery), two sham-HST and three HST gilts received V, while three HST gilts received pulses of 2.5 micrograms GnRH every 45 min for 8 days. At 1200 on Day 5, all gilts, including three unoperated controls (UC), received 1,000 IU of PMSG im. Blood was sampled from all but UC gilts every 15 min from 0800 to 0845 on Days 1 through 5. Ovarian data were obtained on Day 9. The HST + V gilts failed to respond to PMSG, whereas growth of ovulatory follicles was stimulated in the other groups in both experiments.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effect of N-methyl-d,l-aspartate on luteinizing hormone secretion in ovariectomized ewes in the absence and presence of estradiol.

N-methyl-d,l-aspartate (NMA), a potent agonist of the neuroexcitatory amino acids aspartate and glutamate, stimulates release of luteinizing hormone (LH) in rats and nonhuman primates. The objective of the experiments described here was to determine the effect of NMA on LH secretion in ovariectomized ewes, in both the absence and presence of estradiol. In Experiment 1, blood samples were collected from 16 ewes every 12 min for 4 h. At Hour 2, ewes received i.v. injections of either 0, 6, 12, or 24 mg NMA/kg body weight dissolved in 0.9% saline (n = 4 per treatment). Mean LH concentrations were unaltered by any dose of NMA (p greater than 0.3). Immediately after completion of Experiment 1, each ewe received an s.c. Silastic implant designed to maintain circulating concentrations of estradiol of approximately 1 pg/ml. Three weeks later, Experiment 2 was conducted, using the same blood sampling regimen and doses of NMA as Experiment 1. The estradiol implants decreased serum LH concentrations in all animals. Treatment with saline failed to alter mean LH concentrations (p greater than 0.3). In contrast, 6, 12, and 24 mg NMA/kg body weight increased mean LH concentrations by 326% (p less than 0.03), 1125% (p less than 0.02), and 441% (p less than 0.0001), respectively. These results demonstrate that exogenous estradiol suppresses LH release in sheep in a manner antagonized by NMA.

Animals↗

Effects of free fatty acids on luteinizing hormone and growth hormone secretion in ovariectomized lambs.

The effects of FFA on circulating LH and GH concentrations in ovariectomized ewe lambs were investigated. Lambs (n = 14) were weaned at 2.5 months, ovariectomized at 6.5 months, and used at 8.5 months of age. From weaning until day 0 of the experiment, lambs were fed to maintain body weights (23 kg). On day 0, serum FFA concentrations and mean serum LH concentrations and number and amplitude of LH pulses, as assessed in blood samples collected every 12 min for 4 h, were 6.4 +/- 0.6 mg/100 ml, 0.57 +/- 0.08 ng/ml, 0.45 +/- 0.09 pulses/h, and 0.73 +/- 0.11 ng/ml, respectively. Double the maintenance feeding, beginning day 1, increased (P less than 0.01) body weights by 16% and LH pulse frequency by 82%, but had no effect (P greater than 0.1) on FFA concentrations, mean LH concentrations, or LH pulse amplitude by day 14. On day 14, lambs were infused with lipid (n = 9; 95.8 mg/min) or 0.9% saline solution (n = 5) for 8 h. Blood samples were collected at 12-min intervals for 12 h, beginning 4 h before infusions. FFA levels increased (P less than 0.01) in lipid-infused animals to 27.6 +/- 2.9 mg/100 ml by 4 h of infusion. Mean LH concentrations and LH pulse frequency and amplitude were unaffected (P greater than 0.1) by treatment. In contrast, mean GH concentrations and GH pulse frequency, which were similar (P greater than 0.1) between groups before infusion (14.0 +/- 0.8 ng/ml and 0.36 +/- 0.07 pulses/h, respectively) were decreased by FFA treatment by 51% (P less than 0.01) and 81% (P less than 0.006), respectively. GH pulse amplitude was highly variable and unaffected (P greater than 0.1) by treatment. In summary, elevated FFA levels appear to inhibit the release of GH, but not LH, in the ovariectomized ewe lamb.

Animals↗

Growth hormone release after N-methyl-D,L-aspartate in sheep: dose response and effect of an opioid antagonist.

The objectives of our experiments were 1) to determine the effect of N-methyl-D,L-aspartate (NMA), an agonist of the neuroexcitatory amino acids aspartate and glutamate, on growth hormone (GH) release in ovariectomized ewes, and 2) to determine the effect of naloxone, an opioid antagonist, on the GH response to NMA. Jugular blood was collected via venipuncture at 12-min intervals for 2 h before and 2 h after i.v. injection of NMA. In Exp. 1, ewes received either 0, 6, 12 or 24 mg NMA/kg BW dissolved in .9% saline solution (n = 4 per treatment). Growth hormone concentrations were similar (P greater than .1) between groups prior to injection (9.8 +/- .7 ng/ml; mean +/- SEM) and were unaffected (P greater than .1) by saline treatment. In contrast, 6, 12 or 24 mg NMA/kg BW increased mean GH concentration by 210% (P less than .04), 273% (P less than .02) and 234% (P less than .02), respectively. In Exp. 2, ewes received NMA (6 mg/kg BW) 5 min after either saline (n = 4) or naloxone (1 mg/kg BW; n = 4) pretreatment. Serum GH concentrations averaged 7.0 +/- 1.1 ng/ml before pretreatment and increased similarly (238%; P greater than .1) in both groups following NMA. In summary, NMA increased GH concentrations in ovariectomized ewes by some mechanism that does not involve opioid receptors that are antagonized by naloxone.

Analysis of Variance↗

Gonadotropin and prolactin secretion following intraventricular administration of morphine in gilts.

The effects of central nervous system administration of morphine on secretion of luteinizing hormone (LH), follicle-stimulating hormone, and prolactin were investigated in ovariectomized gilts stereotaxically implanted with lateral ventricular cannulas. In Experiment 1, mean serum LH and follicle-stimulating hormone concentrations and serum LH pulse frequency were unaffected by artificial cerebrospinal fluid administration (P greater than 0.1), but decreased (P less than 0.01) in 8 of 11 gilts when 500 micrograms of morphine were given 3 hr later. Serum LH pulse amplitude was unaffected (P greater than 0.1) by cerebrospinal fluid or morphine injection. In Experiment 2, luteinizing hormone concentrations decreased (P less than 0.0001) and prolactin concentrations increased (P less than 0.0001), but follicle-stimulating hormone concentrations did not change (P greater than 0.1) after 500 micrograms of morphine. Gonadotropin responses to 10 micrograms of gonadotropin-releasing hormone, given 2 hr after intraventricular injection, were similar (P greater than 0.1) for morphine- and cerebrospinal fluid-treated gilts. These results indicate that morphine inhibits LH secretion at the level of the central nervous system, and are consistent with the concept that endogenous opioid peptides participate in the regulation of gonadotropin and prolactin release in pigs.

Analysis of Variance↗

Effects of age on fasting-induced changes in insulin, glucose, urea nitrogen, and free fatty acids in sera of sheep.

The hypothesis that prepubertal ewe lambs are metabolically different from postpubertal ewes was tested. Ovariectomized ewes (4 years of age; n = 4) and lambs (6 months of age; n = 4) were fasted for 72 hr. Serum concentrations of insulin, glucose, urea nitrogen, and free fatty acids (FFA) were measured in blood samples taken at 6-hr intervals between 30 hr before and 72 hr after feed removal. Serum concentrations of urea nitrogen and glucose were not different (P greater than 0.20) between age groups before fasting. Serum concentrations of insulin in ewes increased toward the end of the prefast period whereas those in lambs did not (age x time, P less than 0.01). Serum concentrations of FFA in ewes tended to be lower (P less than 0.07) than those in lambs prior to fasting. During fasting, concentrations of insulin decreased (P less than 0.02) over time in ewes and lambs and did so in a similar manner (age x time, P greater than 0.70). Urea nitrogen increased (P less than 0.0001) in both fasted ewes and fasted lambs in a comparable manner (age x time, P greater than 0.20). Concentrations of glucose during fasting were not significantly affected (P greater than 0.90) by age. There was a tendency (P = 0.08) for concentrations of glucose to change over time but the pattern did not appear to be related to fasting. During fasting, concentrations of FFA tended to be higher (P less than 0.07) in lambs than in ewes and increased (P less than 0.0001) in both groups in a similar fashion (age x time, P greater than 0.10). The findings herein suggest that turnover of FFA in lambs may be slightly greater than that in ewes during the fed and fasted states.

Age Factors↗

N-methyl-d, l-aspartate stimulates growth hormone but not luteinizing hormone secretion in the sheep.

The objective of this experiment was to determine the effects of N-methyl-d, l-aspartate (NMA) on luteinizing hormone (LH) and growth hormone (GH) secretion in castrated male sheep. Blood was sampled from Hampshire wethers every 15 min for 8 hr on day 1. At 4 and 6 hr after the initiation of the experiment, wethers were treated i.v. with NMA at a dose of 12 mg/kg body weight (n = 5) or .9% saline (n = 5). The dosage of NMA was within the range of doses that was previously demonstrated to stimulate LH secretion in monkeys. Blood samples were also collected every 15 min for 1 hr on day 2, beginning 24 hr after the first injection of NMA or saline. Treatment with NMA had no effect on mean LH concentrations, LH pulse frequency or LH pulse amplitude during the 4 hr period following the first injection on day 1. On day 2, however, mean LH concentrations were lower (p less than .01) in NMA versus saline-treated wethers. Conversely, administration of NMA evoked a dramatic increase (p less than .02) in mean GH concentrations on day 1. The mechanisms responsible for the effects of NMA described herein and whether or not these effects are relevant to the physiological control of LH and GH release in the sheep warrants further scrutiny.

Animals↗

Luteinizing hormone and prolactin secretion in hypophysial-stalk-transected pigs given estradiol and pulsatile gonadotropin-releasing hormone.

To determine the sites of action whereby estradiol (E2) induces the preovulatory luteinizing hormone (LH) surge in pigs, hypophysial-stalk-transected (HST) ovariectomized (OVX) gilts (mean +/- SE: 118 +/- 12 kg) received intramuscular injections of E2 benzoate (10 micrograms E2B/kg body weight) on day 0, plus intravenous pulses of 1 microgram gonadotropin-releasing hormone (GnRH) every 45 min either from days -5 to 4, days -5 to 0 or days -5 to 0 then days 2 to 4. A fourth and fifth group received steroid vehicle on day 0 and pulses of GnRH on either days -5 to 4 or days -5 to 0 then days 2 to 4. In stalk-intact OVX gilts, E2B inhibited LH release for 48 h, then induced an LH surge that peaked 60-84 h after steroid treatment. In HST OVX gilts, serum LH increased from undetectable concentrations (less than 0.17 ng/ml) to 0.42 +/- 0.03 ng/ml after 5 days of pulsatile GnRH replacement. In the presence of pulsatile GnRH stimulation, serum LH concentrations were inhibited for 12 h after E2B but then returned to values that were similar to those for HST gilts given GnRH in the absence of steroid treatment. Discontinuing GnRH pulses at the time of E2B injection caused serum LH concentrations to drop to 0.18 ng/ml or less for the remaining 96 h. When GnRH pulses were interrupted for 48 h, beginning immediately after injecting E2B or vehicle to mimic the secretory hiatus of LH and presumably GnRH observed in stalk-intact pigs prior to the surge, resumption of GnRH pulses caused serum LH concentrations to increase progressively over 3 h in E2B-treated gilts but to peak abruptly in controls given vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Free fatty acids suppress growth hormone, but not luteinizing hormone, secretion in sheep.

An experiment was conducted to determine the effects of exogenously administered FFA on GH and LH secretion in sheep. Ovariectomized ewes received iv infusions of a mixture of FFA (166 mg/min; n = 5) or 0.9% saline (n = 4) for 10 h. Jugular blood was sampled every 15 min for 14 h, beginning 4 h before initiation of infusion. After 8 h of FFA or saline treatment, each ewe received a pituitary challenge of 10 micrograms GRF and 1 microgram GnRH, administered together as an iv bolus. Lipid infusion increased (P less than 0.01) serum FFA concentrations to levels characteristic of those in fasted sheep [23.0 +/- 0.8 mg/100 ml (mean +/- SE)]. Frequency of GH pulses (P less than 0.01) and the GH response to GRF (P less than 0.0001) were suppressed by FFA treatment. Mean serum GH concentrations increased gradually (P less than 0.01) during the 10-h infusion period in saline-treated but not lipid-treated, ewes. This finding may reflect diurnal changes in somatotrope secretory activity that are blocked by FFA. Mean serum LH concentrations, LH pulse frequency and amplitude, and the LH secretory response to GnRH were unaffected by FFA or saline infusion. In agreement with previous work in sheep and other species, these results provide evidence for an inhibitory effect of FFA on GH release. The exact mechanism responsible for this action, however, remains to be elucidated. Finally, acutely elevated FFA levels do not appear to influence LH secretion in the ovariectomized ewe.

Animals↗

Long-term liquid storage of porcine spermatozoa separated using a discontinuous bovine serum albumin gradient.

Two experiments were conducted to determine efficacy of a discontinuous bovine serum albumin (BSA) gradient for isolating viable porcine spermatozoa more tolerant to 5-d liquid storage in Beltsville Thawing Solution (BTS) at 15 degrees C. The gradient, contained in a 500-ml separatory funnel, consisted of 4% BSA (60 ml) over 10% BSA (60 ml). Spermatozoa were extended in 26 ml of BTS, layered on top of the gradient, and allowed to migrate through the BSA. The quality of spermatozoa separated by the gradient varied among boars. However, populations of spermatozoa isolated from the bottom 30 ml of the gradient (Fraction 4) consistently contained a high percentage of spermatozoa with acrosomes possessing normal apical ridges (NAR; 89.6%) and progressively motile spermatozoa (MOT; 84.0%), as well as spermatozoa with high velocity (VEL; 336.5 mu/s). Increasing sperm migration time, but not gradient temperature, increased the number of spermatozoa recovered in Fraction 4, but it did not reduce quality of the separated spermatozoa. Spermatozoa isolated in Fraction 4 had greater NAR, MOT and VEL after 5-d storage in BTS than did unseparated spermatozoa. Boar spermatozoa isolated on a discontinuous BSA gradient were more tolerant to storage at 15 degrees C than were unseparated spermatozoa. Such a population may be desirable for use in artificial insemination programs.

Acrosome↗

Effects of recombinant DNA-derived somatotropin and dietary energy intake on development of beef heifers: II. Concentrations of hormones and metabolites in blood sera.

The effects of somatotropin (STH) and energy intake on serum concentrations of glucose (GLU), insulin (INS), nonesterified fatty acids (NEFA), urea nitrogen (UN) and insulin-like growth factor-I (IGF-I) were determined in 40 Angus heifers. At 7 mo (208 +/- 8 d) of age heifers were assigned to four treatment groups: 1) vehicle (V) + high energy (HE; 2.68 Mcal ME/kg DM), 2) recombinant DNA-derived STH (20.6 mg/d; s.c.) + HE, 3) V + low energy (LE; 2.22 Mcal ME/kg DM) or 4) STH + LE. Animals remained on treatments until an average of 15.5 mo of age. Blood samples were taken every 30 min for 4 h at 9, 11, 13 and 15 mo of age to determine circulating concentrations of metabolites and hormones. Serum IGF-I was increased (P less than .01) by STH injections, but this effect appeared to diminish with age (STH x age; P less than .01). Energy intake did not influence IGF-I levels. Somatotropin increased (P less than .01) serum GLU in heifers fed the HE diet but only tended (P = .08) to increase GLU in those fed the LE diet (STH x energy; P = .05). Although STH increased (P less than .01) serum INS in both energy groups, the response in heifers fed the HE diet was greater (P less than .02) than that in heifers fed the LE diet (STH x energy; P less than .05). Heifers fed LE had higher (P less than .01) concentrations of NEFA than heifers fed HE.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

Luteinizing hormone secretion in hypophysial stalk-transected pigs given progesterone and pulsatile gonadotropin-releasing hormone.

This study was conducted to determine whether progesterone inhibits luteinizing hormone (LH) secretion in female pigs by a direct action on the pituitary gland. Eight ovariectomized, hypophysial stalk-transected gilts were given 1-microgram pulses of gonadotropin-releasing hormone iv every 45 min from Day 0 to 12. On Days 5-12, each of four gilts received either progesterone or oil vehicle im at 12-hr intervals. Serum progesterone concentrations in steroid-treated gilts reached 70 +/- 6.8 ng/ml (mean +/- SE) by Day 8 and remained elevated thereafter, whereas serum progesterone concentrations in oil-treated controls were less than 1 ng/ml for the entire study. Daily serum LH concentrations were not different between gilts treated with progesterone or oil. The 1-microgram pulses of gonadotropin-releasing hormone reliably evoked pulses of LH in both treatment groups. The LH pulse frequency and amplitude, assessed from samples collected every 15 min for 6 hr on Day 12, were similar for progesterone- and oil-treated gilts. These results provide evidence that progesterone does not act at the pituitary gland to alter LH secretion in pigs.

Animals↗