Effect of human growth hormone-releasing factor and(or) thyrotropin-releasing factor on hormone concentrations in dairy calves

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)     

Dose effect of human growth hormone-releasing factor and thyrotropin-releasing factor on hormone concentrations in lactating dairy cows

Two experiments were conducted to study the effects of growth hormone-releasing factor (GRF) and thyrotropin-releasing factor (TRF) administration on hormone concentrations in dairy cows. In the first trial, 12 cows were used on 5 consecutive days to determine the effect of four sc doses of GRF (0, 1.1, 3.3 and 10 μg•kg⁻¹ BW) and three sc doses of TRF (0, 1.1 and 3.3 μg•kg⁻¹ BW) combined in a factorial arrangement. GRF and TRF acted in synergy (P = .02) on serum growth hormone (GH) concentration even at the lowest dose tested and GH response to the two releasing factors was higher than the maximal response observed with each factor alone. TRF increased (P<.01) prolactin (Prl), thyrotropin (TSH), triiodothyronine (T₃) and thyroxine (T₄) concentrations similarly at the 1.1 and 3.3 μg•kg⁻¹ doses and GRF did not interact (P>.40) with TRF on the release of these hormones. In the second trial, the effect of GRF (3.3 μg•kg⁻¹ BW, sc) and TRF (1.1 μg•kg⁻¹ BW, sc) was tested at three stages (18, 72 and 210 days) of lactation on serum Prl and TSH concentrations. Eighteen cows (n = 6 per stage of lactation) were used in two replicates of a 3 × 3 latin square. The TRF and GRF-TRF treatments were equipotent (P>.05) in increasing Prl and TSH concentrations. Prl and TSH responses were similar (P>.40) throughout lactation. In summary, GRF at doses ranging from 1.1 to 10.0 μg•kg⁻¹ and TRF at doses ranging from 1.1 to 3.3 μg•kg⁻¹ act in synergy on GH release and do not interact on Prl, TSH, T₃ and T₄ concentrations in dairy cows. Furthermore, Prl and TSH response to TRF are not affected by stage of lactation.     

Concentrations of insulin-like growth factor I and steroids in follicular fluid of preovulatory bovine ovarian follicles: effect of daily injections of a growth hormone-releasing factor analog and(or) thyrotropin-releasing hormone

To determine whether long-term administration of growth hormone (GH)-releasing factor (GRF) and(or) thyrotropin-releasing hormone (TRH) alters ovarian follicular fluid (FFL) concentrations of insulin-like growth factor-I (IGF-I), progesterone, and estradiol (E2), and follicular growth, Friesian x Hereford heifers (n = 47; 346 +/- 3 kg) were divided into the following four groups: control (vehicle; n = 11); 1 micrograms GRF (human [Des NH2 Tyr1, D-Ala2, Ala15] GRF [1-29]-NH2).kg-1 BW.d-1 (n = 12); 1 microgram TRH.kg-1 BW.d-1 (n = 12); or GRF + TRH (n = 12). Daily injections (s.c.) continued for 86 d. On d 89, heifers that had been synchronized were slaughtered and ovaries were removed. Follicles were grouped by magnitude of diameter into the three following sizes: 1 to 3.9 mm (small, n = 55), 4.0 to 7.9 mm (medium, n = 63), and greater than or equal to 8 mm (large, n = 71). Growth hormone-releasing factor and(or) TRH did not affect (P greater than .10) IGF-I concentrations in FFL of any follicle size group. Growth hormone-releasing factor increased (P less than .06) size (means +/- pooled SE) of large follicles (14.7 vs 13.0 +/- .6 mm). Growth hormone-releasing factor also increased (P less than .05) progesterone concentrations 4.4-fold above controls in FFL of medium-sized follicles but had no effect on progesterone in FFL of the small or large follicles. Thyrotropin-releasing hormone did not alter FFL progesterone or E2 concentrations in any follicle size group. We conclude that the GRF and(or) TRH treatments we employed did not affect intra-ovarian IGF-I concentrations, but GRF may alter steroidogenesis of medium-sized follicles and growth of large follicles.     

Effect of long-term administration of human growth hormone-releasing factor and (or) thyrotropin-releasing factor on hormone concentrations in lactating dairy cows

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.     

Growth hormone secretory responsiveness to multiple injections of growth hormone-releasing factor in sheep

Growth hormone releasing factor (GRF) has been shown to be a potent and specific stimulant of growth hormone (GH) secretion in a variety of species. The objective of this series of experiments was to determine whether repeated iv bolus injections of GRF would increase circulating levels of GH, and thus have the potential to stimulate growth in young lambs. In lambs given three injections of hpGRF either one (.065 nmol/Kg) or two hours apart (.016 or .065 nmol/Kg), the GH secretory responses decreased significantly with each subsequent injection. Bolus injections of hpGRF (.016 nmol/Kg) given for three days in 15 Kg lambs resulted in development of refractoriness to subsequent injections. In lambs treated three and six times daily, basal plasma GH and SmC levels decreased progressively over the three day period. Older lambs (30 Kg) also became less responsive to hpGRF given once daily for three days, but the refractoriness was less pronounced than in 15 Kg lambs. In 30 Kg lambs treated once daily with bovine GRF (bGRF, .065 nmol/Kg), GH secretory responsiveness decreased progressively over a five day treatment period. Because of the severe refractoriness to GRF that developed in very young lambs, it was predicted that multiple injections over several weeks might result in suppression of growth. However, growth rate, feed intake and feed efficiency were not altered in 10 Kg lambs treated twice daily for three weeks with .065 nmol/Kg bGRF and there was no evidence of refractoriness to bGRF as determined every seven days. These results suggest that the refractoriness that develops with multiple bolus injections of GRF may not be long-lasting, and therefore will not have a negative impact on growth. However, there was no evidence that at the frequencies tested bolus injections of GRF could stimulate growth in young lambs.     

Effect of long-term administration of porcine growth hormone-releasing factor and(or) thyrotropin-releasing factor on growth hormone, prolactin and thyroxine concentrations in growing pigs

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.     

Effects of somatostatin immunoneutralization on growth and endocrine parameters in chickens

The effects of somatostatin immunoneutralization on growth rate, growth hormone (GH) secretion and circulating insulin-like growth factor I (IGF-I) concentrations were investigated in chickens through the use of passive and active immunization techniques. Intravenous bolus injection of goat-antisomatostatin stimulated a significant (P less than .05) increase in plasma GH levels for one hour post-injection in four and six week old male broiler chickens. The GH response to an intravenous bolus injection of hGRF44NH2 was similar in the antisomatostatin treated chicks and normal goat serum treated controls. Despite the presence of circulating somatostatin antisera after 28 hours, plasma GH levels were not different between control and antisomatostatin-treated chicks at that time. Continuous administration of somatostatin antisera by Alzet pump over a two-week period resulted in significant (P less than .05) elevations in plasma GH levels at one week post-implantation and in circulating IGF-I concentrations after two weeks of administration. Chicks which developed antibodies against somatostatin following active immunization exhibited a 7.1% increase in growth rate which was associated with a significant decrease in abdominal fat. However, neither GH nor IGF-I concentrations were elevated in the chicks which developed somatostatin antibodies. Thus, the benefits gained from somatostatin immunoneutralization may be exerted through mechanisms other than GH.     

Synergism and diurnal variations of human growth hormone-releasing factor (1-29)NH2 and thyrotropin-releasing factor on growth hormone release in dairy calves

Sixteen male Holstein calves averaging 168 kg body weight (BW) were used to determine the effects of human growth hormone-releasing factor (1–29)NH₂ (hGRF (1–29)NH₂; .22 μg/kg BW), thyrotropin-releasing factor (TRF; .165 μg/kg BW) or hGRF (1–29)NH₂ plus TRF (.22 and .165 μg/kg BW, respectively) on growth hormone (GH) release in animals exposed to 16 hr of light (L): 8 hr of dark (D) (lights on at 0100 hr) and hGRF plus TRF (.22 and .165 μg/kg BW, respectively) in animals exposed to 8L:16D (lights on at 0900 hr). For each treatment, times of iv injection were 0400, 1000, 1600 and 2200 hr. In animals exposed to 16L:8D, average GH peaks reached after hGRF (1–29)NH₂ or TRF injections were 49.7 and 32.0 ng/ml while the area under the GH response curve (AUC) were 1247 and 1019 ng/ml^*min, respectively. There was no significant effect of times of injection on GH release following the separate injection of hGRF (1–29)NH₂ or TRF. In animals exposed to 16L:8D, GH peaks and AUC after hGRF plus TRF injections were 226.4, 189.2 and 116.8 ng/ml, and 4340, 3660 and 2415 ng/ml^*min at 0400, 1000 and 1600 hr (lights on), respectively but only 42.3 ng/ml and 1692 ng/ml^*min at 2200 hr (lights off). In animals exposed to 8L:16D, GH levels and AUC after hGRF plus TRF injections reached 177.5 and 180.5 ng/ml, and 2759 and 3704 ng/ml^*min at 1000 and 1600 hr (lights on) but only 84.0 and 72.7 ng/ml, and 1544 and 1501 ng/ml^*min at 0400 and 2200 hr (lights off), respectively. These results demonstrated that hGRF (1–29)NH₂ and TRF can act in synergy to potentiate GH release in dairy calves. This synergistic action occurred only when both peptides were injected during the lighted phase of short and long day photoperiods.     

Stimulation of pig growth performance by porcine growth hormone and growth hormone-releasing factor

The current study was undertaken to determine the effects of human growth hormone-releasing factor [hpGRF-(1-44)-NH2] on growth performance in pigs and whether this response was comparable to exogenous porcine growth hormone (pGH) treatment. Preliminary studies were conducted to determine if GRF increased plasma GH concentration after iv and im injection and the nature of the dose response. Growth hormone-releasing factor stimulated the release of pGH in a dose-dependent fashion, although the individual responses varied widely among pigs. The results from the im study were used to determine the dose of GRF to use for a 30-d growth trial. Thirty-six Yorkshire-Duroc barrows (initial wt 50 kg) were randomly allotted to one of three experimental groups (C = control, GRF and pGH). Pigs were treated daily with 30 micrograms of GRF/kg body weight by im injection in the neck. Pigs treated with pGH were also given 30 micrograms/kg body weight by im injection. Growth rate was increased 10% by pGH vs C pigs (P less than .05). Growth rate was not affected by GRF; however, hot and chilled carcass weights were increased 5% vs C pigs (P less than .05). On an absolute basis, adipose tissue mass was unaffected by pGH or GRF. Carcass lipid (percent of soft-tissue mass) was decreased 13% by GRF (P less than .05) and 18% by pGH (P less than .05). Muscle mass was significantly increased by pGH but not by GRF. There was a trend for feed efficiency to be improved by GRF; however, this was not different from control pigs. In contrast, pGH increased feed efficiency 19% vs control pigs (P less than .05). Chronic administration of GRF increased anterior pituitary weight but did not affect pituitary GH content or concentration. When blood was taken 3 h post-injection, both GRF- and pGH-treated pigs had lower blood-urea nitrogen concentrations. Serum glucose was significantly elevated by both GRF and pGH treatment. This was associated with an elevation in serum insulin. These results indicate that increasing the GH concentration in blood by either exogenous GH or GRF enhances growth performance. The effects of pGH were more marked than for GRF. Further studies are needed to determine the optimal dose of GRF to administer in growth trials and the appropriate pattern of GRF administration in order to determine whether GRF will enhance pig growth performance to the extent that exogenous pGH does.     

The influence of growth hormone injections on the endocrine and metabolic status of gilts

Twelve Yorkshire x Landrace prepubertal gilts were assigned equally to treatments involving daily injections of either porcine growth hormone (GH, 90 micrograms/kg) or vehicle buffer from 150 to 159 d of age. Blood samples were obtained every hour from 0600 hr at 153 d until 0500 hr at 154 d of age, inclusively. At 0800 hr on 154 d, gilts received an injection of 500 IU PMSG, followed 96 hr later by 250 IU hCG. Gilts were slaughtered at 163 d and the ovaries recovered for an assessment of the ovarian response to the gonadotrophic stimulation. Five control gilts (83%) exhibited a normal ovulatory response but only one GH gilt (17%) was so designated (P less than 0.05). There was no apparent effect of treatment on serum concentrations of LH, FSH or cortisol. Growth hormone treatment reduced serum concentrations of T4 (P less than 0.001) and prolactin (P less than 0.02), but increased serum GH (P less than 0.001), T3 (P less than 0.06), insulin (P less than 0.001) and glucose (P less than 0.001). Serum concentrations of free fatty acids (FFA) were not significantly altered by exogenous GH. The concomitant elevation of serum insulin and glucose suggests that an insulin-resistant state was induced which, if evident at the ovarian level, may be a factor mediating the adverse effects of exogenous GH on ovarian function. The data presented also suggests that circulating concentrations of thyroid originating hormones are altered by exogenous GH.     

Growth hormone response to a novel growth hormone-releasing tripeptide in horses: interaction with gonadotropin-releasing hormone, thyrotropin-releasing hormone, and sulpiride

A series of experiments was performed to determine the factor(s) responsible for an apparent inhibition of GH secretion in mares administered the GH secretagogue EP51389 in combination with GnRH, thyrotropin-releasing hormone (TRH), and sulpiride. Experiment 1 tested the repeatability of the original observation: 10 mares received EP51389 at 10 microg/kg BW; five received TRH (10 microg/kg BW), GnRH (1 microg/kg BW), and sulpiride (100 microg/kg BW) immediately before EP51389, and five received saline. The mixture of TRH, GnRH, and sulpiride reduced (P = 0.0034) the GH response to EP51389, confirming the inhibitory effects. Experiment 2 tested the hypothesis that sulpiride, a dopamine antagonist, was the inhibitory agent. Twelve mares received EP51389 as in Exp. 1; six received sulpiride before EP51389 and six received saline. The GH responses in the two groups were similar (P > 0.1), indicating that sulpiride was not the inhibitory factor. Experiment 3 tested the effects of TRH and(or) GnRH in a 2 x 2 factorial arrangement of treatments. Three mares each received saline, TRH, GnRH, or the combination before EP51389 injection. There was a reduction (P < 0.0001) in GH response in mares receiving TRH, whereas GnRH had no effect (P > 0.1). Given those results, Exp. 4 was conducted to confirm that TRH was inhibitory in vivo as opposed to some unknown chemical interaction of the two compounds in the injection solution. Twenty mares received TRH or saline and(or) EP51389 or saline in a 2 x 2 factorial arrangement of treatments. Injections were given separately so that the two secretagogues never came in contact before injection. Again, TRH reduced (P < 0.0001) the GH response to EP51389. In addition, TRH and EP51389 each resulted in a temporary increase in cortisol concentrations. Experiment 5 tested whether TRH would alter the GH response to GHRH itself. Twelve mares received porcine GHRH at 0.4 microg/kg BW; six received TRH prior to GHRH and six received saline. After adjustment for pretreatment differences between groups, the GHRH-induced GH response was completely inhibited (P = 0.068) by TRH. Exp. 6 was a repeat of Exp. 5, except geldings were used (five per group). Again, pretreatment with TRH inhibited (P < 0.0001) the GH response to GHRH. In conclusion, TRH inhibits the GH response not only to EP51389 but also to GHRH in horses, and in addition to its known secretagogue action on prolactin and TSH it may also stimulate ACTH at the dosage used in these experiments.     

Active immunization of pigs against growth hormone-releasing factor: effect on concentrations of growth hormone and insulin-like growth factor 1

Cyclic gilts (96 +/- 1 kg) were used to determine the effect of active immunization against growth hormone-releasing factor GRF(1-29)-NH2 on concentrations of growth hormone (GH) and insulin-like growth factor 1 (IGF-1). Gilts were immunized against GRF conjugated to human serum albumin (GRF-HSA, n = 5) or HSA alone at 180 d of age (wk 0). Booster doses were administered at wk 9 and 13. Seven days after the second booster (wk 14), blood samples were collected at 15-min intervals for 6 h before feeding and 30, 60, 120, 180 and 240 min after feeding. Eight days after the second booster, all gilts were administered a GRF analog, [desNH2Tyr1,Ala15]-GRF(1-29)-NH2, followed by an opioid agonist, FK33-824. Blood samples were collected at 15-min intervals from -30 to 240 min after injection. Immunization against GRF-HSA resulted in antibody titers, expressed as dilution required to bind 50% of [125I]GRF, ranging from 1:11,000 to 1:60,000 (wk 11 and 14); binding was not detectable or was less than 50% at 1:100 in HSA gilts (P less than .05). Episodic release of GH was abolished by immunization against GRF-HSA (P less than .05). Mean GH was decreased (P less than .07), but basal GH concentrations were not altered (P greater than .15) by immunization against GRF-HSA. Serum concentrations of IGF-1 were similar at wk 0, but concentrations were lower in GRF-HSA than in HSA gilts (P less than .05) at wk 14.(ABSTRACT TRUNCATED AT 250 WORDS)     

Energy relationships in growing chickens given daily injections of corticosterone

1. The energetic efficiency of growing chickens given daily injections of corticosterone was investigated by measuring metabolic activity and energy balance.

2. Water consumption increased significantly within the first day of treatment ; food consumption increased by the third day of treatment.

3. Growth rate, which was suppressed during the first two days, returned to normal by the third day of treatment.

4. Excreted water, dry matter and uric acid increased within the first day of treatment.

5. Heat production was not changed by treatment; however, the CO₂:O₂ respiratory ratio (RQ) was increased by the third day and exceeded 1·0 on days 4 and 5 of treatment.

6. Leg muscle weight was decreased and abdominal fat and liver weight were increased by corticosterone treatment.

7. Balance data indicated that energy absorption efficiency was decreased and energy retention efficiency was increased by corticosterone treatment, confirming the RQ, and carcase findings that greater amounts of energy were stored as fat.

     

Effect of human growth hormone-releasing factor and(or) thyrotropin-releasing factor on growth, carcass composition, diet digestibility, nutrient balance, and plasma constituents in dairy calves

Sixty male dairy grain-fed calves, raised from 70 to 223 kg BW in individual crates, were used in a 2 X 2 factorial arrangement to determine the effect of administration of human growth hormone-releasing factor (1-29)NH2 (GRF) and(or) thyrotropin-releasing factor (TRF). Calves received twice-daily s.c. injections of .9% NaCl (control), GRF (5 micrograms/kg BW), TRF (1 micrograms/kg BW) or GRF (5 micrograms/kg BW) plus TRF (1 micrograms/kg GTRF). Average daily gain and days on feed were not affected by treatments, but TRF treatment increased (P less than .05) total intake of dry matter (DM) and feed conversion ratio: 3.00, 3.02, 3.08, and 3.22 kg DM/kg weight gain for control, GRF, TRF, and GTRF, respectively. During two 7-d periods, after 66 and 75 d of treatment, feces and urine were collected from 40 calves (5 per treatment per period). Treatment with GRF increased (P less than .05) digestibility of DM, nitrogen (N), and energy and tended (P less than .20) to increase N retention. At slaughter, withers height was increased (P = .05) by GRF and carcass length was increased (P less than .05) by TRF. Pituitary and liver weights were increased (P less than .05) by TRF. The combination of GRF and TRF slightly increased (P less than .10) protein content and decreased (P less than .05) fat content of the 9-10-11th rib section. After d 1, GRF treatment chronically increased (P less than .05) insulin concentrations and also increased (P less than .10) IGF-I concentrations on d 29 and 57. In summary, chronic treatment with GRF and(or) TRF did not improve growth or efficiency, although GRF increased digestibility of DM, N, and energy and the GRF plus TRF combination resulted in slightly leaner carcasses.     

不同品种鸡生长期与攻击行为前后期TRH和TH激素含量的对比分析

为探讨下丘脑-垂体-甲状腺轴对斗鸡攻击行为的影响,采用免疫组织化学法对比分析不同生长阶段吐鲁番斗鸡与新罗曼蛋鸡下丘脑中促甲状腺激素释放激素(TRH)神经元的数量,结合酶联免疫吸附法测定两品种成年公鸡攻击行为表现前、中、后各时期血清中TRH和甲状腺激素(TH)的含量。结果表明两品种鸡的TRH在下丘脑中的阳性细胞数随着周龄增加而减少,整体上吐鲁番斗鸡TRH的阳性细胞数高于新罗曼蛋鸡,公鸡高于母鸡;斗鸡和新罗曼蛋鸡血清中TRH的含量随着周龄增加逐渐上升,TH呈下降趋势,且吐鲁番斗公鸡的TRH和TH含量较高,打斗时间的持续性也比新罗曼蛋公鸡长。因此,吐鲁番斗鸡较强的攻击行为可能与这两种激素含量偏高有关。     

Effect of dose and frequency of administration of a potent analog of human growth hormone-releasing factor on hormone secretion and growth in pigs

Ninety-six pigs (49.5 +/- .5 kg BW) were allotted to six treatments and were injected once (SID) or three times daily (TID) s.c. with a [desamino-Tyr1, D-Ala2, Ala15] human growth hormone-releasing factor (1-29) NH2 analog (GRF-AN). Treatments were T1, noninjected control; T2, saline-injected control (TID); T3, GRF-AN (1.66 micrograms/kg BW, TID); T4, GRF-AN (3.33 micrograms/kg BW, TID); T5, GRF-AN (6.66 micrograms/kg BW, TID) and T6, GRF-AN (10 micrograms/kg BW, SID). Feed protein levels were 14% for T1 and 18.8% for T2 through T6. The GRF-AN increased serum growth hormone (GH) concentration for the entire growing period (about 56 d) in a dose-related manner and did not induce desensitization of the somatotroph cells; in fact, an increase (P less than .05) in the GH response to GRF-AN was observed in T4 and T5 after 1 mo of treatment. This GRF-AN produced (P less than .05) a dose-dependent effect on several variables in animals grown to 110 kg BW: in comparison to T2, T5 increased meat in carcass (6%), carcass length (3%), loin eye area (13%), liver weight (19%), kidney weight (30%), improved feed efficiency (20%) and decreased total feed intake by 50 kg (26%). Compared to T2, average daily gain was increased (P less than .05) by 13% by the 3.33 micrograms/kg TID dose. Blood parameters were measured on d 1, 29 and 57. Increased serum glucose and insulin levels were observed. Triiodothyronine and thyroxine concentrations were increased and decreased, respectively after 28 d of treatment but were unchanged on d 57. This potent GRF analog maintained high GH concentration for at least 56 d and affected several growth parameters and carcass characteristics in a dose-related manner similar in magnitude to that reported in studies using porcine GH.     

Analogs of growth hormone-releasing hormone induce release of growth hormone in the bovine

Biological potencies of three 29 amino acid growth hormone-releasing hormone analogs (GHRH[1-29]) were determined in the bovine and compared to synthetic human GHRH (44 amino acids; hGHRH[1-44]NH2) for their ability to increase serum growth hormone (GH) concentrations. Four prepubertal Holstein heifers (179 +/- 10 kg) received hGHRH(1-44)NH2 or analogs (D-Ala2, Nle27, Agm29 GHRH[1-29], [JG-73]; D-N-MeAla2, Nle27, Agm29 GHRH[1-29], [JG-75]; and desamino-Tyr1, D-Ala2, Nle27, Agm29 GHRH[1-29], [JG-77]) at the following doses: 0, 6.25, 25, 100 and 400 micrograms/animal. All treatment-dose combinations were administered to each heifer with at least a 1-d interval between treatments. Sixteen blood samples were collected via jugular cannulas 20 min before and up to 6 h after treatment injection. There was a linear dose-dependent GH release in response to hGHRH(1-44)NH2 and the three analogs. Growth hormone peak amplitudes for the three analogs were similar to those observed after administration of the hGHRH(1-44)NH2 (P greater than .05). However, when total area under the GH response curves for each treatment was averaged over all the doses, JG-73 stimulated greater GH release than hGHRH(1-44)NH2 (P less than .05) Heifers injected with the 400-microgram dose of hGHRH(1-44)NH2 or the three analogs showed a primary release of GH followed by a secondary release 1 h later. At all other doses, only a primary GH release was observed.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of oral chlortetracycline and dietary protein level on plasma concentrations of growth hormone and thyroid hormones in beef steers before and after challenge with a combination of thyrotropin-releasing hormone and growth hormone-releasing hormone.

The objective of this study was to determine the effect of a subtherapeutic level of chlortetracycline (CTC) fed to growing beef steers under conditions of limited and adequate dietary protein on plasma concentrations of GH, thyroid-stimulating hormone (TSH), and thyroid hormones before and after an injection of thyrotropin-releasing hormone (TRH) + GHRH. Young beef steers (n = 32; average BW = 285 kg) were assigned to a 2x2 factorial arrangement of treatments of either a 10 or 13% crude protein diet (70% concentrate, 15% wheat straw, and 15% cottonseed hulls) and either a corn meal carrier or carrier + 350 mg of CTC daily top dressed on the diet. Steers were fed ad libitum amounts of diet for 56 d, and a jugular catheter was then placed in each steer in four groups (two steers from each treatment combination per group) during four consecutive days (one group per day). Each steer was injected via the jugular catheter with 1.0 microg/kg BW TRH + .1 microg/kg BW GHRH in 10 mL of saline at 0800. Blood samples were collected at -30, -15, 0, 5, 10, 15, 20, 30, 45, 60, 120, 240, and 360 min after releasing hormone injection. Plasma samples were analyzed for GH, TSH, thyroxine (T4), and triiodothyronine (T3). After 84 d on trial, the steers were slaughtered and the pituitary and samples of liver were collected and analyzed for 5'-deiodinase activity. Feeding CTC attenuated the GH response to releasing hormone challenge by 26% for both area under the response curve (P<.03) and peak response (P<.10). Likewise, CTC attenuated the TSH response to releasing hormone challenge for area under the response curve by 16% (P<.10) and peak response by 33% (P<.02), and attenuated the T4 response for area under the curve by 12% (P<.08) and peak response by 14% (P<.04). Type II deiodinase activity in the pituitary was 36% less (P<.02) in CTC-fed steers than in steers not fed CTC. The results of this study are interpreted to suggest that feeding subtherapeutic levels of CTC to young growing beef cattle attenuates the release of GH and TSH in response to pituitary releasing hormones, suggesting a mechanism by which CTC may influence tissue deposition in cattle.     

Effect of human growth hormone-releasing factor on bone and mineral metabolism in growing pigs

Little information is available on the effects of growth hormone (GH) and growth hormone-releasing factor (GRF and GHRH) treatment on bone metabolism in pigs. Thus, tibial bending moments and ash contents were studied in 12, 6-wk-old pigs weighing 13 +/- .2 kg. Six pigs (GRF group) were injected s.c. twice daily with 75 micrograms GRF (hGRF [1-29] NH2)/kg BW for 52 d and six remained untreated (control group, C). Average daily gain was slightly (5%; P less than .10) increased in treated pigs. At slaughter, plasma measurements related to calcium homeostasis, such as concentrations of Ca, inorganic P, and vitamin D metabolites (25-OH and 1,25-(OH)2 vitamin D3), were not changed by GRF injection. At slaughter, plasma GH levels were 3.3 times greater in treated (11.3 +/- 3 ng/ml) than in untreated pigs (3.4 +/- .5 ng/ml, P less than .02), whereas those of insulin-like growth factor I were increased by approximately 38%. No difference was observed between the two groups at slaughter in tibial weight, density, bending moment, ash relative to bone volume (29 +/- 1 vs 30 +/- 2 g/100 cm3, GRF vs C), total ash content, or ash relative to dry matter in cortical or medullary bone. Our GRF treatment did not affect bone and mineral metabolism in young, growing pigs.