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1.
Sixteen ovariectomized (OVX) mature gilts, averaging 139.6 ± 3.1 kg body weight (BW) were assigned randomly to receive either progesterone (P, 0.85 mg/kg BW, n=8) or corn oil vehicle (OIL, n=8) injections im twice daily for 10 d. On the day of experiment, all gilts received either the EAA agonist, N-methyl-d,l-aspartate (NMA; 10 mg/kg BW, iv) alone or NMA plus the EOP antagonist, naloxone (NAL, 1 mg/kg BW, iv), resulting in the following groups of 4 gilts each: OIL-NMA, OIL-NMA-NAL, P-NMA and P-NMA-NAL. Blood samples were collected via jugular cannula every 15 min for 6 hr. All pigs received NMA 5 min following pretreatment with either 0.9% saline or NAL 2 hr after blood collection began and a GnRH challenge 3 hr after NMA. Administration of NMA suppressed (P<0.03) LH secretion in OIL-NMA gilts and treatment with NAL failed to reverse the suppressive effect of NMA on LH secretion in OIL-NMA-NAL gilts. Similar to OIL-NMA gilts, NMA decreased (P<0.03) mean serum LH concentrations in P-NMA gilts. However, in P-NMA-NAL gilts, serum LH concentrations were not changed following treatment. All gilts responded to GnRH with increased (P<0.01) LH secretion. Additionally, administration of NMA increased (P<0.01) growth hormone (GH) and prolactin (PRL) secretion in both OIL-NMA and P-NMA gilts, but this increase in GH and PRL secretion was attenuated (P<0.01) by pretreatment with NAL in OIL-NMA-NAL and P-NMA-NAL gilts. Serum cortisol concentrations increased (P<0.01) in all gilts and the magnitude of the cortisol response was not different among groups. In summary, results of the present study confirmed previous findings that NMA suppresses LH secretion in both oil- and P-treated OVX gilts, but we failed to provide definitive evidence that EOP are involved in the NMA-induced suppression of LH secretion. However, NMA may, in part, activate the EOP system which in turn increased GH and PRL secretion in the gilt.  相似文献   

2.
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)  相似文献   

3.
To test the hypothesis that orexin-B acts directly on the anterior pituitary to regulate LH and growth hormone (GH) secretion, anterior pituitary cells from prepuberal gilts were studied in primary culture. On day 4 of culture, 10(5) cells/well were challenged with 0.1, 10 or 1000 nM GnRH; 10, 100 or 1000 nM [Ala15]-hGRF-(1-29)NH2 or 0.1, 1, 10 or 100 nM, orexin-B individually or in combinations with 0.1 and 1000 nM GnRH or 10 and 1000 nM GRF. Secreted LH and GH were measured at 4 h after treatment. Basal LH and GH secretion (control; n = 6 pigs) was 183 +/- 18 and 108 +/- 4.8 ng/well, respectively. Relative to control at 4 h, all doses of GnRH and GRF increased (P < 0.0001) LH and GH secretion, respectively. All doses of orexin-B increased (P < 0.01) LH secretion, except for the 0.1 nM dose. Basal GH secretion was unaffected by orexin-B. Addition of 1, 10 or 100 nM orexin-B in combinations with 0.1 nM GnRH increased (P < 0.001) LH secretion compared to GnRH alone. Only 0.1 nM (P = 0.06) and 100 nM (P < 0.001) orexin-B in combinations with 1000 nM GnRH increased LH secretion compared to GnRH alone. All doses of orexin-B in combination with 1000 nM GRF suppressed (P < 0.0001) GH secretion compare to GRF alone, while only 0.1 nM orexin-B in combination with 10 nM GRF suppressed (P < 0.01) GH secretion compared to GRF. These results indicate that orexin may directly modulate LH and GH secretion at the level of the pituitary gland.  相似文献   

4.
Thirty-five ovariectomized pony mares were used to study the relationships among luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) concentrations in blood (secretion), in pituitary (storage) and in blood after secretagogue administration, as well as the content of gonadotropin releasing hormone (GnRH) in hypothalamic areas, under various conditions of steroidal and nonsteroidal treatment. Five mares each were treated daily for 21 d with vegetable shortening (controls), testosterone (T; 150 micrograms/kg of body weight, BW), dihydrotestosterone (DHT; 150 micrograms/kg BW), estradiol (E2; 35 micrograms/kg BW), progesterone (P4; 500 micrograms/kg BW), dexamethasone (DEX; 125 micrograms/kg BW) or charcoal-stripped equine follicular fluid (FF; 10 ml). Secretagogue injections (GnRH and thyrotropin releasing hormone, TRH, at 1 and 4 micrograms/kg of BW, respectively) were given one d prior to treatment and again after 15 d of treatment. Relative to controls, treatment with T, DHT and DEX reduced (P less than .05) LH secretion, storage and response to exogenous GnRH, whereas treatment with E2 increased (P less than .05) these same characteristics. Treatment with P4 reduced (P less than .05) only LH secretion. Treatment with T, DHT, E2 and DEX reduced (P less than .05) FSH secretion, whereas treatment with P4 increased (P less than .05) it and FF had no effect (P greater than .1). All treatments increased (P less than .05) FSH storage, whereas only treatment with T and DHT increased (P less than .05) the FSH response to exogenous GnRH. Other than a brief increase (P less than .05) in PRL secretion in mares treated with E2, secretion of PRL did not differ (P greater than .1) among groups. Only treatment with E2 increased (P less than .01) PRL storage, yet treatment with T or DHT (but not E2) increased (P less than .05) the PRL response to exogenous TRH. Content of GnRH in the body and pre-optic area of the hypothalamus was not affected (P greater than .1) by treatment, whereas treatment with T, E2 and DEX increased (P less than .1) GnRH content in the median eminence. For LH, secretion, storage and response to exogenous GnRH were all highly correlated (r greater than or equal to .77; P less than .01). For FSH, only storage and response to exogenous GnRH were related (r = .62; P less than .01). PRL characteristics were not significantly related to one another. Moreover, the amount of GnRH in the median eminence was not related (P greater than .1) to any LH or FSH characteristic.  相似文献   

5.
Three experiments were conducted to determine the effects of n-methyl-D,L-aspartate (NMA), an agonist of the excitatory amino acid glutamate, on secretion of hormones in boars. In Exp. 1, boars (185.0+/-.3 d of age; mean +/- SE) received i.v. injections of either 0, 1.25, 2.5, 5, or 10 mg of NMA/kg BW. There were no effects of NMA (P>.1) on secretion of LH and testosterone. Treatment with NMA, however, increased (P<.01) circulating GH concentrations in a dose-dependent manner. In Exp. 2, boars (401 d of age) received an i.v. challenge of NMA at a dose of 10 mg/kg BW or .9% saline. Treatment with NMA, but not saline (P>.1), increased serum concentrations of LH (P<.01), GH (P <.01), and testosterone (P<.06). In Exp. 3, boars that were 152, 221, or 336 d of age were treated i.v. with NMA (10 mg/kg BW). Across ages, treatment with NMA increased circulating concentrations of LH (P<.07) and testosterone (P<.01). However, NMA increased (P<.01) mean GH concentrations in only the oldest boars. Treatment with NMA had no effect (P>.1) on circulating concentrations of estradiol or leptin; however, estradiol concentrations increased (P<.03) with age. In summary, NMA increased secretion of LH, GH, and testosterone in boars. However, endocrine responses to treatment with NMA may be influenced by age of the animal. Finally, NMA did not influence circulating concentrations of estradiol or leptin.  相似文献   

6.
Effect of age and intake on growth hormone kinetics in dairy heifers.   总被引：2，自引：0，他引：2  
The effects of aging and intake on growth hormone (GH) kinetics and GH-releasing factor (GRF)-induced GH concentrations were studied in two groups of 12 Holstein heifers each (80 d, 85 kg: young; and 273 d of age, 246 kg: old). Each group was then equally subdivided into full-fed (FF) and restricted-fed (RF) subgroups. After 11 d of intake treatment, animals were infused for 3 hr with GH (1.5 mg/hr) in order to calculate GH metabolic clearance rate (MCR), secretion rate (SR) and half-life (t 1/2). Two d later, total plasma volume was determined and the following day, all heifers received a GRF challenge (5 micrograms/kg i.v.). The following values are LSM +/- SE for young-FF, young-RF, old-FF and old-RF. Rate of secretion was not affected by any treatment, averaging 1.51, 1.25, 1.34, and 1.40 +/- .23 micrograms/min. Aging increased (P < .01) MCR (186, 159, 382, and 300 +/- 21 ml/min) and increased plasma volume (P < .01), which resulted in lower basal GH concentrations. Aging also decreased (P < .01) the area under the GH response curve following GRF injection (AUC: 12442, 21114, 5155, and 6308 +/- 1776 ng.min/ml) but did not affect average GH quantity in the plasma after the GRF challenge. Feed restriction decreased (P < .05) MCR, but not enough to affect basal GH concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

7.
Twelve long-term ovariectomized (OVX) pony mares were used to determine the effects of dexamethasone (DEX) or progesterone (PR) on concentrations of follicle stimulating hormone (FSH) and luteinizing hormone (LH) in daily blood samples and after administration of gonadotropin releasing hormone (GnRH). All mares were subsequently administered dihydrotestosterone (DHT) to determine if DEX or PR treatment altered the FSH or LH response to this androgen. Daily blood sampling was started on day 1. After a pretreatment injection of GnRH on day 5, four mares were administered DEX at 125 micrograms/kg of body weight (BW), four mares were administered PR at 500 micrograms/kg of BW and four mares were administered vehicle. Injections were given subcutaneously in vegetable shortening daily through day 14. After a second injection of GnRH on day 15, all mares were administered DHT in shortening at 150 micrograms/kg of BW. Injections of DHT were given daily through day 24. A final injection of GnRH was given on day 25. Treatment of mares with DEX 1) reduced (P less than .01) daily LH secretion and briefly increased (P less than .05) daily FSH secretion and 2) increased (P less than .01) the FSH response to exogenous GnRH. Treatment of mares with PR had no effect on daily LH secretion but increased (P less than .05) daily FSH secretion and increased (P less than .01) the FSH response to exogenous GnRH.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

8.
Two experiments were conducted in ovariectomized, pituitary stalk-transected ewes to determine if dopamine (DA), norepinephrine (NE) or serotonin (5-HT) alter secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL). In experiment 1, ewes were infused (iv) with saline (control), DA (66 micrograms/kg/min), NE (6.6 micrograms/kg/min) or 5-HT (6.6 micrograms/kg/min). Treatments did not alter pulse frequency, but 5-HT increased (P less than .05) amplitude of pulses of LH and mean concentrations of LH, DA and NE were without effect on basal secretion of LH. DA but not NE or 5-HT decreased (P less than .05) the release of LH in response to gonadotropin hormone-releasing hormone (GnRH, 25 micrograms, im). Concentrations of FSH were not affected by treatments. Secretion of PRL was reduced (P less than .05) by treatment with DA and NE but not 5-HT. Each amine reduced (P less than .05) the release of PRL in response to thyrotropin-releasing hormone (TRH; 3 micrograms, im). In experiment 2, ewes were given DA at doses of 0, 0.66, 6.6 or 66.0 micrograms/kg/min, iv. No dose altered basal LH, but each dose reduced (P less than .05) basal and TRH-induced release of PRL. Key findings from these studies include direct pituitary action for: (1) 5-HT enhanced basal secretion of LH, (2) suppression of GnRH-induced secretion of LH by DA. (3) DA and NE inhibition of PRL secretion, and (4) DA, NE and 5-HT inhibition of release of PRL in response to TRH.  相似文献   

9.
Long-term administration of porcine growth hormone-releasing factor (pGRF(1-29)NH2) and(or) thyrotropin-releasing factor (TRF) was evaluated on serum concentrations of growth hormone (GH) thyroxine (T4) and prolactin (PRL). Twenty-four 12-wk-old female Yorkshire-Landrace pigs were injected at 1000 and 1600 for 12 wk with either saline, pGRF (15 micrograms/kg), TRF (6 micrograms/kg) or pGRF + TRF using a 2 x 2 factorial design. Blood samples were collected on d 1, 29, 57 and 85 of treatment from 0400 to 2200. Areas under the GH, T4 and PRL curves (AUC) for the 6 h (0400 to 1000) prior to injection were subtracted from the postinjection periods (1000 to 1600, 1600 to 2200) to calculate the net hormonal response. The AUC of GH for the first 6 h decreased similarly (P less than .05) with age for all treatments. The GH response to GRF remained unchanged (P greater than .10) across age. TRF alone did not stimulate (P less than .05) GH release but acted in synergy with GRF to increase (P less than .05) GH release. TRF stimulated (P less than .001) the net response of T4 on all sampling days. Animals treated with the combination of GRF + TRF showed a decreased T4 AUC during the first 6 h on the last three sampling days. Basal PRL decreased (P less than .05) with age. Over the four sampling days, animals injected with TRF alone showed (P less than .01) a reduction (linear effect; P less than .01) followed by an increase (quadratic effect; P less than .05) in total PRL concentration after injection; however, when GRF was combined with TRF, such effects were not observed (P greater than .10). Results showed that 1) chronic injections of GRF for 12 wk sustained GH concentration, 2) TRF and GRF acted synergistically to elevate GH AUC, 3) TRF increased T4 concentrations throughout the 12-wk treatment period, 4) chronic TRF treatment decreased the basal PRL concentration and 5) chronic GRF + TRF treatment decreased the basal concentration of T4.  相似文献   

10.
Fifteen cows (87 +/- 8 d in lactation; 641 +/- 33 kg BW) were randomly assigned to treatment and then subjected for 182 d to daily sc injection (1000 hr), in the cervical area, of saline (control), thyrotropin-releasing factor (TRF: 1 micrograms/kg BW), growth hormone-releasing factor (1-29)NH2 (GRF; 10 micrograms/kg BW) or GRF plus TRF (10 and 1 micrograms/kg BW, respectively) according to a 2 x 2 factorial design. On days 1, 31, 88 and 179, jugular blood samples were collected from 2 hr before to 6 hr after injection. Samples were also collected for 5 consecutive days after cessation of treatment. GRF always induced growth hormone (GH) release (600 vs 7925 ng.min/ml) with augmentation of response with time (interaction GRF * day; P less than .001). TRF did not affect (P greater than .25) GH release; there was no interaction (P greater than .25) with time. There was no significant interaction (P greater than .25) between GRF and TRF on GH release. However, the amount of GH release with GRF plus TRF was always greater than with GRF alone (9419 vs 6431 ng.min/ml). TRF induced a significant release of prolactin (23769 vs 42175 ng.min/ml) but GRF reduced the amount of prolactin release on the last day of sampling. TRF induced thyroid stimulating hormone (TSH) release only on the first day of injection while triiodothyronine (T3) and thyroxine (T4) continued to respond to TRF throughout the treatment period. Concentrations of T3 and T4 fell below control levels after cessation of TRF injection. In conclusion, GRF-induced GH release and TRF-induced Prl and thyroid hormone release were maintained over a 6-mo treatment period. TRF induced TSH release only on the first day of injection. Overall, these results raised the possibility of a direct effect of TRF on the thyroid gland.  相似文献   

11.
Photoperiod modulates reproduction in goats. We tested the hypothesis that the excitatory glutamatergic tone is reduced in the photoinhibited goat. The objectives of this study were to determine the effect of photoperiod and glutamatergic stimulation on LH, GH, and testosterone (T) secretion in goat bucks. Eight mature, intact bucks were used in two simultaneous 4 x 4 Latin square designs. Variables were two photoperiod regimens (short day; SD, 10 h light:14 h dark, n = 4; vs long day; LD, 16 h light:8 h dark, n = 4) and four doses of N-methyl-D-L-aspartate (NMA; 0, 1, 2 and 4 mg/kg BW, i.v.). Venous blood was obtained for 2 h before and after NMA injection, followed by GnRH injection and then a final 1 h of sampling. Injection of NMA increased (P < 0.002) LH secretion within 20 min. This increase was sustained for 120 min, but the response was most pronounced in LD goats. The increase in mean LH was associated with a concomitant dose-dependent increase in pulse frequency (P < 0.006). However, NMA treatment had no effect (P > 0.10) on LH pulse amplitude. The release of LH after injection of GnRH was not affected by photoperiod. Exposure of bucks to LD reduced T secretion relative to that of SD bucks (P < 0.01). However, GH secretion was enhanced in LD bucks (P< 0.001). The response of GH to NMA was dependent on photoperiod history. A highly significant immediate and sustained increase (P < 0.001) was observed in LD but not in SD bucks within 10 min. Overall, a dose-dependent increase (P < 0.01) in T secretion was stimulated by NMA in both LD and SD bucks. These results indicate that NMA receptors may be involved in the regulation of LH, GH, and testosterone secretion in the goat. Furthermore, length of day influences GH secretion in the goat and NMA receptor activation had divergent effects on the secretion of this hormone.  相似文献   

12.
Opioid modulation of LH and prolactin (PRL) concentrations in Angus steers was investigated. In Exp. 1, morphine sulfate (M) was administered at either 1, 2 or 3 mg/kg BW (n = 4) as an i.v. injection. Blood samples were obtained at 15-min intervals for 4 h pre- and post-treatment for serum hormone analyses. Mean serum LH concentration and number of LH secretory pulses decreased (P less than .1) for 2 h after M (4.1 to nadir of 2.4 ng/ml, and .33 vs. .21 pulses/h; pre- vs post-treatment). Luteinizing hormone pulse amplitude decreased (P less than .01; 7.3 vs 2.6 ng/ml; pre- vs post-treatment) during the 2 h following M. Prolactin concentrations increased 126.6%, 170.6% and 187.6% following 1, 2 and 3 mg M/kg BW, respectively (P less than .05, 1 vs 2; P less than .01, 1 vs 3). In Exp. 2, either saline solution (S, n = 6) or M (.31 mg/kg BW, i.v. injection followed by .15 mg/(kg.h) infusion; n = 6) was given for 7 h. Concentration of LH was unaffected. Response of LH to naloxone was determined in Exp. 3. Blood samples were obtained for 2 h pre- and post-administration of either naloxone (1 mg/kg BW, i.v. injection; n = 5) or S (n = 5). Response of LH at 15, 30 and 45 min posttreatment was greater (P less than .05) in naloxone- compared with S-treated steers. In summary, M had no significant effect on serum LH concentration or LH pulse frequency, but it decreased pulse amplitude and increased serum PRL concentrations. In contrast, naloxone increased LH secretion. These observations taken together indicate a physiological role for opioid modulation of LH and PRL secretion in the steer.  相似文献   

13.
Two experiments (Exp) were conducted to examine in vitro the release of gonadotropin releasing hormone (GnRH) from the hypothalamus after treatment with naloxone (NAL) or morphine (MOR). In Exp 1, hypothalamic-preoptic area (HYP-POA) collected from 3 market weight gilts at sacrifice and sagitally halved were perifused for 90 min prior to a 10 min pulse of morphine (MOR; 4.5 × 10−6 M) followed by NAL (3.1 × 10−5 M) during the last 5 min of MOR (MOR + NAL; N=3). The other half of the explants (n=3) were exposed to NAL for 5 min. Fragments were exposed to KCl (60 mM) at 175 min to assess residual GnRH releasability. In Exp 2, nine gilts were ovariectomized and received either oil vehicle im (V; n=3); 10 μg estradiol-17β/kg BW im 42 hr before sacrifice (E; n=3); .85 mg progesterone/kg BW im twice daily for 6 d prior to sacrifice (P4; n=3). Blood was collected to assess pituitary sensitivity to GnRH (.2 μg/kg BW) on the day prior to sacrifice. On the day of sacrifice HYP-POA explants were collected and treated as described in Exp 1 except tissue received only NAL. In Exp 1, NAL increased (P<.05) GnRH release. This response to NAL was attenuated (P<.05) by coadministration of MOR. Cumulative GnRH release after NAL was greater (P<.05) than after MOR + NAL. All tissues responded similarly to KCl with an increase (P<.05) in GnRH release. In Exp 2, pretreatment luteinizing hormone (LH) concentrations were lower (P<.05) in E gilts compared to V and P4 animals with P4 being lower (P<.05) than V gilts. LH response to GnRH was lower (P<.05) in E pigs than in V and P4 animals, while the responses was similar between V and P4 gilts. NAL increased GnRH release in all explants, whereas, KCl increased GnRH release in 6 of 9 explants. These results indicate that endogenous opioid peptides may modulate in vitro GnRH release from the hypothalamus in the gilt.  相似文献   

14.
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.  相似文献   

15.
Pituitary cells, from seven 160- to 170-day-old pigs, were studied in primary culture to determine the affects NPY on LH and GH secretion at the level of the pituitary. On day 4 of culture, medium was discarded, plates were rinsed twice with serum-free medium and cells were cultured in 1 ml fresh medium without serum and challenged individually with 10(-10), 10(-8) or 10(-6) M [Ala(15)]-h growth hormone-releasing factor-(1-29)NH(2) (GRF); 10(-9), 10(-8) or 10(-7) M GnRH or 10(-9), 10(-8), 10(-7) or 10(-6) M NPY individually or in combinations with 10(-9) or 10(-8) M GnRH or 10(-8) or 10(-6)M GRF. Cells were exposed to treatment for 4 h at which time medium was harvested and quantified for LH and GH. Basal LH secretion (control; n = 7 pituitaries) was 12 +/- 6 ng/well. Relative to control at 4 h, 10(-9), 10(-8) and 10(-7) M GnRH increased (P < 0.01) LH secretion by 169, 176 and 197%, respectively. Neuropeptide-Y did not alter (P > 0.4) basal LH secretion nor 10(-8) M GnRH-induced increase in LH secretion but 10(-9) M GnRH-stimulated LH secretion was reduced by NPY and was not different from control or GnRH alone. Basal GH secretion (control; n = 7 pituitaries) was 56 +/- 12 ng/well. Relative to control at 4 h, 10(-10), 10(-8) and 10(-6) M GRF increased GH secretion by 111%, 125% (P < 0.01) and 150% (P < 0.01), respectively. Only 10(-6) M (134%) and 10(-7) M (125%) NPY increased (P < 0.04) basal GH secretion. Addition of 10(-9), 10(-8) and 10(-7) M NPY in combination with 10(-8) M GRF suppressed (P < 0.04) GRF-stimulated GH secretion. However, 10(-9) M NPY enhanced (P < 0.06) the GH response to 10(-6) M GRF. These results demonstrate that NPY may directly modulate GH secretion at the level of the pituitary gland.  相似文献   

16.
To determine the effect of chronic treatment with human growth hormone-releasing factor (1-29)NH2 (GRF) and(or) thyrotropin-releasing factor (TRF), 20 calves averaging 70.2 kg BW were divided into four groups (n = 5) according to a 2 X 2 factorial design. For 86 d, calves in each group received twice daily s.c. injections of either .9% NaCl, GRF (5 micrograms/kg BW), TRF (1 microgram/kg BW) or GRF (5 micrograms/kg BW) plus TRF (1 microgram/kg BW). On d 87, all calves received a s.c. injection of GRF (5 micrograms/kg BW) plus TRF (1 microgram/kg BW). Blood samples were collected every 20 min for 18 h on d 1, 29, 57 and 85, and for 8 h on d 87. Hormone responses were measured as area under the hormone concentration curve over time. GRF and TRF acted in synergy (P less than .10) on GH release throughout the treatment period. Growth hormone responsiveness to GRF and(or) TRF decreased (P less than .01) with days of treatment, but this decrease was due to aging rather than to chronic treatment, because GH response to GRF plus TRF was similar (P greater than .10) between control and treated calves on d 87. TRF increased prolactin (Prl) concentration until the end of the treatment period (P less than .01). The response of thyroid-stimulating hormone (TSH) to TRF disappeared (P greater than .10) after 1 mo of treatment, whereas the thyroxine (T4) response decreased (P less than .01) throughout the treatment period. GRF did not induce nor did it interact with TRF on TSH and T4 release.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

17.
Thirty-nine adult light horse mares, geldings, and stallions were used in two experiments to assess the pituitary hormone and insulin responses to infusions of arginine, aspartic acid, lysine, glutamic acid, and N-methyl-D,L-aspartate (NMA). In Exp. 1, 27 horses were assigned to one of three infusion treatments: 1) physiological saline (1 L); 2) 2.855 mmol of arginine/kg BW in 1 L of water; or 3) 2.855 mmol of aspartic acid/kg BW in 1 L of water. In Exp. 2, 12 horses were assigned, in a multiple-square 4 x 4 Latin square design, to one of four infusion treatments: 1) 2 mL of saline/kg BW; 2) 2.855 mmol of lysine/kg BW in water; 3) 2.855 mmol of glutamic acid/kg BW in water; or 4) 1 mg of NMA/kg BW in water. In Exp. 1, an acute (within 20 min) release of growth hormone (GH) was induced (P = 0.002) by aspartic acid. In contrast, acute release of prolactin (P = 0.001) and insulin (P = 0.002) was induced only by arginine; moreover, the arginine effect on insulin was present only in mares (P = 0.011). In Exp. 2, an acute release of GH was induced (P = 0.001) by glutamic acid and NMA. In males, the glutamic acid-induced GH release was greater than that of NMA; in mares, the NMA-induced GH release was greater than that of glutamic acid (P = 0.069). Both lysine and glutamic acid induced (P = 0.001) acute release of prolactin, whereas an acute release of insulin was elicited (P = 0.002) only by lysine. The NMA-induced LH response was due almost entirely to the response in mares and stallions (P = 0.016), and the NMA-induced FSH release was due almost entirely to the response in mares (reproductive status effect; P = 0.004). In the horse, aspartic acid, glutamic acid, and NMA seem to stimulate GH release; arginine and lysine seem to stimulate prolactin and insulin release; and NMA seems to stimulate LH and FSH release. It seems that N-methyl-D-aspartate glutamate receptors are involved in controlling GH, LH, and FSH secretion, whereas other mechanisms are involved with prolactin secretion. These results also indicate that gonadal steroids interact with amino acid-induced pituitary hormone release in adult horses.  相似文献   

18.
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.  相似文献   

19.
Two experiments were performed to examine the influence of exogenous growth hormone on the reproductive axis in gilts. Experiment one employed 26 Yorkshire × Landrace prepubertal gilts, which were selected at 150 d and 86.5 ± 1.5 kg bodyweight (BW) and assigned equally to two treatments. Gilts received injections of either porcine growth hormone at 90 μg/kg BW, or vehicle buffer, from 150 to 159 d. At 154 d gilts received 500 IU PMSG, followed 96 hr later by 250 IU hCG. Gilts were slaughtered at 163 days and their ovaries recovered to determine ovulatory status. In each treatment, gilts failed to show any ovarian response to PMSG/hCG. All remaining control gilts ovulated and their ovaries appeared morphologically normal. In gilts receiving exogenous growth hormone, fewer ovaries (4/11, P<.01) appeared morphologically normal. The ovaries of all other growth hormone injected gilts had very large (12–25 mm) non-luteinized follicles. In experiment two, 20 prepubertal Yorkshire × Landrace gilts were selected at 138 days and 85 kg BW. These gilts received injections of growth hormone at 90 μg/kg BW (n=9) or vehicle (n=11) from 138 to 147 days. At 143 days, all gilts were given an injection of estradiol benzoate (EB) at 15 μg/kg BW. Blood samples were taken at the time of EB injection, at 24 and 36 hr and then at 6 hr intervals until 78 hr. All samples were assayed for serum LH concentrations. The EB induced LH peak height was lower (P<.04) in gilts receiving exogenous growth hormone than in controls. The results presented indicate that the daily injection of growth hormone at 90 μg/kg BW reduced the estradiol-induced release of LH in addition to reducing the number of corpora lutea in gonadotrophin stimulated gilts.  相似文献   

20.
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.  相似文献   

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