Growth and carcass characteristics and serum growth hormone, prolactin and insulin profiles in Debouillet lambs treated with ovine growth hormone and(or) zeranol

Sixteen Debouillet wether lambs (approximately 3 mo old) were placed indoors in 1.5- x 3-m pens (14 h light:10 h dark) 28 d after weaning. Lambs received no implant or a 12-mg zeranol implant on d-2 (eight lambs/group). Two days later (d 0), animals received either 0 or 2.5 mg ovine growth hormone (oGH, eight lambs/group) s.c. on alternate days for 42 d. Animals had ad libitum access to water, salt, mineral and a pelleted alfalfa diet (16% CP). After 42 d, lambs were slaughtered to evaluate carcass traits, organ weights and femur characteristics. Zeranol by oGH interactions were not detected (P greater than .20). Zeranol increased (P less than .05) BW, improved (P less than .05) feed:gain during the first 20 d and increased (P less than .10) feed intake during the last 22 d of the 42-d trial compared with controls. Carcass characteristics were not altered (P greater than .10) by 12 mg zeranol. Serum insulin and prolactin were elevated (P less than .05), but serum GH was not influenced by zeranol compared with controls. Exogenous oGH decreased feed intake (P less than .10) and improved feed:gain (P less than .05) during the initial 20 d compared with controls, but did not influence (P greater than .20) these variables during the last 22 d of the study. Carcass traits were not influenced (P greater than .10) by oGH. Exogenous ovine GH dramatically elevated (P less than .05) serum GH, but did not affect serum insulin or prolactin (P greater than .10).(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyrotropin releasing hormone interactions with growth hormone secretion in horses

Light horse mares, stallions, and geldings were used to 1) extend our observations on the thyrotropin releasing hormone (TRH) inhibition of GH secretion in response to physiologic stimuli and 2) test the hypothesis that stimulation of endogenous TRH would decrease the normal rate of GH secretion. In Exp. 1 and 2, pretreatment of mares with TRH (10 microg/kg BW) decreased (P < 0.001) the GH response to exercise and aspartate infusion. Time analysis in Exp. 3 indicated that the TRH inhibition lasted at least 60 min but was absent by 120 min. Administration of a single injection of TRH to stallions in Exp. 4 increased (P < 0.001) prolactin concentrations as expected but had no effect (P > 0.10) on GH concentrations. Similarly, 11 hourly injections of TRH administered to geldings in Exp. 5 did not alter (P > 0.10) GH concentrations either during the injections or for the next 14 h. In Exp. 5, it was noted that the prolactin and thyroid-stimulating hormone responses to TRH were great (P < 0.001) for the first injection, but subsequent injections had little to no stimulatory effect. Thus, Exp. 6 was designed to determine whether the inhibitory effect of TRH also waned after multiple injections. Geldings pretreated with five hourly injections of TRH had an exercise-induced GH response identical to that of control geldings, indicating that the inhibitory effect was absent after five TRH injections. Retrospective analysis of pooled, selected data from Exp. 4, 5, and 6 indicated that endogenous GH concentrations were in fact lower (P < 0.01) from 45 to 75 min after TRH injection but not thereafter. In Exp. 7, 6-n-propyl-2-thiouracil was fed to stallions to reduce thyroid activity and hence thyroid hormone feedback, potentially increasing endogenous TRH secretion. Treated stallions had decreased (P < 0.01) concentrations of thyroxine and elevated (P < 0.01) concentrations of thyroid-stimulating hormone by d 52 of feeding, but plasma concentrations of GH and prolactin were unaffected (P > 0.10). In contrast, the GH response to aspartate and the prolactin response to sulpiride were greater (P < 0.05) in treated stallions than in controls. In summary, TRH inhibited exercise- and aspartate-induced GH secretion. The duration of the inhibition was at least 1 h but less than 2 h, and it waned with multiple injections. There is likely a TRH inhibition of endogenous GH episodes as well. Reduced thyroid feedback on the hypothalamic-pituitary axis did not alter basal GH and prolactin secretion.     

Growth hormone stimulates protein synthesis in bovine skeletal muscle cells without altering insulin-like growth factor-I mRNA expression

Growth hormone is a major stimulator of skeletal muscle growth in animals, including cattle. In this study, we determined whether GH stimulates skeletal muscle growth in cattle by direct stimulation of proliferation or fusion of myoblasts, by direct stimulation of protein synthesis, or by direct inhibition of protein degradation in myotubes. We also determined whether these direct effects of GH are mediated by IGF-I produced by myoblasts or myotubes. Satellite cells were isolated from cattle skeletal muscle and were allowed to proliferate as myoblasts or induced to fuse into myotubes in culture. Growth hormone at 10 and 100 ng/mL increased protein synthesis in myotubes (P < 0.05), but had no effect on protein degradation in myotubes or proliferation of myoblasts (P > 0.05). Insulin-like growth factor-I at 50 and 500 ng/mL stimulated protein synthesis (P < 0.01), and this effect of IGF-I was much greater than that of GH (P < 0.05). Besides stimulating protein synthesis, IGF-I at 50 and 500 ng/mL also inhibited protein degradation in myotubes (P < 0.01), and IGF-I at 500 ng/mL stimulated proliferation of myoblasts (P < 0.05). Neither GH nor IGF-I had effects on fusion of myoblasts into myotubes (P > 0.1). These data indicate that GH and IGF-I have largely different direct effects on bovine muscle cells. Growth hormone at 10 and 100 ng/mL had no effect on IGF-I mRNA expression in either myoblasts or myotubes (P > 0.1). This lack of effect was not because the cultured myoblasts or myotubes were not responsive to GH; GH receptor mRNA was detectable in them and the expression of the cytokine-inducible SH2-containing protein (CISH) gene, a well-established GH target gene, was increased by GH in bovine myoblasts (P < 0.05). Overall, the data suggest that GH stimulates skeletal muscle growth in cattle in part through stimulation of protein synthesis in the muscle and that this stimulation is not mediated through increased IGF-I mRNA expression in the muscle.     

Luteinizing hormone and growth hormone secretion in ewes infused intracerebroventricularly with neuropeptide Y

Neuropeptide Y (NPY) provides an important hypothalamic link between nutritional status and neuroendocrine mechanisms regulating growth and reproduction. The objective of the following series of experiments was to determine the effects of single or continuous administration of NPY on secretion of luteinizing hormone (LH) and (or) growth hormone (GH). In experiment 1, four ovariectomized (OVX) ewes and four OVX + estrogen-treated ewes each received, in a 4 x 4 Latin Square arrangement of treatments, a single injection of 0, 0.5, 5, or 50 microg NPY via an intracerebroventricular (i.c.v.) cannulae to determine the effects on secretion of GH. NPY significantly elevated serum GH at the 50 microg dose regardless of estrogen exposure (P = 0.003). In experiment 2, eight OVX ewes were infused i.c.v. with NPY or saline (n = 4/trmt) continuously for 20 h in a linearly increasing dose, ending at 50 microg/h NPY. Blood samples were collected via jugular cannulae every 10 min during hour -4-0 (interval 1, pre-treatment), hour 6-10 (interval 2) and hour 16-20 (interval 3) relative to the initiation of infusion (0 h). Mean LH and LH pulse frequency were lower in NPY- versus saline-infused ewes during intervals 2 and 3 (P < 0.01), but NPY had no discernable effect on serum GH (P > 0.10). In experiment 3, four OVX ewes were continuously infused with NPY as in experiment 2, except that the maximum 50 microg/h dose was achieved after only 10 h of infusion. Blood samples were collected every 10 min, beginning 4 h before and continuing until 4h after the NPY infusion. Mean serum LH changed significantly over time (P = 0.0001), decreasing below pre-treatment levels by hour 3 of NPY infusion (P < 0.01), and returning to pre-treatment concentrations following the end of infusion (P > 0.15). Serum GH also changed significantly over time (P < 0.001). Mean GH levels tended to be greater than pre-treatment levels by hour 2 of infusion (P < 0.08), but thereafter returned to basal levels. Serum GH also increased following the end of NPY infusion (P < 0.03). From these data we conclude that NPY exerts a persistent inhibitory effect on secretion of LH, and may stimulate the secretion of GH during the initiation and cessation of infusion of NPY. These observations support a role for NPY in mediating the effects of undernutrition on both LH and GH, and also provide evidence for potential mechanisms by which leptin, acting through NPY, may stimulate the secretion of GH.     

The effect of the beta-adrenergic agonist clenbuterol on growth and protein metabolism in rat muscle cell cultures.

Cultures were established from neonatal rat muscle cells, satellite cells, and L6 myoblasts and changes in protein metabolism were determined as development proceeded. For all three cell types, culture protein content increased with increasing myotube content. The beta-adrenergic agonist clenbuterol (added to a final concentration of 10(-7) M) significantly stimulated fusion (as indicated by creatine kinase activity) in neonatal muscle cultures and also increased culture protein content. This was associated with a stimulation in both the fractional (ks, percentage/day, +13%, P less than .05) and absolute (As, micrograms/day, +19%, P less than .05) rates of protein synthesis within 24 h after drug administration. At 48 h, As was increased by 42% above that of controls (P less than .01). In contrast, in satellite cell cultures, clenbuterol had no consistent effects on either protein accretion, creatine kinase activity, or protein synthesis (ks and As). Similarly, the drug had no stimulatory effect on protein synthesis and protein accretion in L6 myoblast or L6 myotube cultures (and no effect in neonatally derived fibroblast cultures). It is concluded that the fusion response to clenbuterol and, therefore, changes in protein metabolism and protein accretion are greatly dependent on the origin and genetic integrity of muscle cells.     

Response to a growth hormone-releasing hormone analog in heifers treated with recombinant growth hormone

Sixteen pregnant Holstein heifers (430kg) were used to determine the effect of long-term administration of a bovine growth hormone (bGH) made by recombinant DNA technology on the ability of a bolus injection of a growth hormone-releasing hormone analog (Ac-His-1, D-Ala-2, Nle-27, GHRH(1-29 NH2) to increase serum GH. Eight heifers received a daily intramuscular injection of bGH (50 mg/day) for 5 months while the other half received a daily injection of physiological saline (control) over the same period. On the last day of bGH treatment and 1, 5, 10 and 25 days after the cessation of bGH treatment, five heifers from each group were challenged with GHRH analog and the response to this releasing hormone analog was measured. Basal GH concentrations were elevated on the last day of treatment in bGH-treated heifers and declined to concentrations similar to control heifers by 1 day after cessation of treatment. Response to GHRH analog was impaired by bGH during the last day of treatment and one day later. Responsiveness returned to a level similar to controls by 5 days after the end of bGH treatment. Response to GHRH analog was lessened during the period of bGH treatment but there were no long term effects on the animals' ability to respond to the releasing hormone.     

Skeletal muscle characteristics in young trained and untrained standardbred trotters.

Muscle biopsies were taken from the middle gluteal muscle of 28 Standardbred trotters, 3-4 years of age. The 13 horses in Group T were trained consistently from 18 months of age, whereas the 15 horses in Group UT were not exposed to any systematic training before 3 years of age. Group T horses had a lower percentage of Type IIB fibres (31%) than did Group UT horses (39%). Citrate synthase (CS) activity, representing oxidative capacity, was higher in Group T (72 mmol kg-1 min-1) than in Group UT (47 mmol kg-1 min-1). Biopsies were taken from 4 horses in each group when they were foals and then annually until 3-4 years of age. Results from this study indicate that regular training of Standardbreds from 18 months of age resulted in increased CS activity and a decrease in the percentage of Type IIB fibres. This study shows that training, not growth, is the main factor that induces a high oxidative capacity and a high Type IIA/IIB fibre ratio in muscle of Standardbred trotters.     

Skeletal muscle protein turnover in broiler and layer chicks

Dietary infusion of L-[U-14C]tyrosine was used to estimate the fractional protein synthesis rates (FSR) in broiler and layer chickens. Six 2-wk-old birds of each strain were placed in individual metabolism cages and given a purified diet in agar-gel containing 2 microCi L-[U-14C]tyrosine for 6 h. The birds were sacrificed and the pectoralis major (PM) and two combined leg (LM) muscles (gastrocnemius and peroneous longus) were removed for analysis. Subgroups of chickens were sacrificed 3 d before and 3 d after infusion to observe changes in muscle composition to calculate fractional protein accretion rates (FAR). Fractional protein breakdown rates (FBR) were calculated by difference (FBR = FSR-FAR). Protein, ribonucleic acid (RNA) and deoxyribonucleic acid (DNA) concentrations were determined to observe relationships between these cellular constituents and FSR. Fractional whole body growth rate and FSR in PM was greater (P less than .05) in broiler than layer birds. The FSR in LM of the layer was not different (P greater than .05) from that of broilers, and from the FSR of the PM in each bird-type. The calculated FBR in the layer PM was at least 17% higher than that of the other muscles. Ratios of FSR to FBR indicated that 16% of the protein synthesized in the layer PM was retained, compared with 45% in the broiler PM. The RNA activity of the layer PM was less (P less than .05) than that of the other muscles investigated. Deoxyribonucleic acid activity was lower (P less than .05) in the PM than LM of either bird-type.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thyrotropin-releasing hormone-induced growth hormone secretion in dogs with primary hypothyroidism

Primary hypothyroidism in dogs is associated with increased release of growth hormone (GH). In search for an explanation we investigated the effect of intravenous administration of thyrotropin-releasing hormone (TRH, 10 microg/kg body weight) on GH release in 10 dogs with primary hypothyroidism and 6 healthy control dogs. The hypothyroid dogs had a medical history and physical changes compatible with hypothyroidism and were included in the study on the basis of the following criteria: plasma thyroxine concentration < 2 nmol/l and plasma thyrotropin (TSH) concentration > 1 microg/l. In addition, (99m)TcO(4)(-) uptake during thyroid scintigraphy was low or absent. TRH administration caused plasma TSH concentrations to rise significantly in the control dogs, but not in the hypothyroid dogs. In the dogs with primary hypothyroidism, the mean basal plasma GH concentration was relatively high (2.3+/-0.5 microg/l) and increased significantly (P=0.001) 10 and 20 min after injection of TRH (to 11.9+/-3.5 and 9.8+/-2.7 microg/l, respectively). In the control dogs, the mean basal plasma GH concentration was 1.3+/-0.1 microg/l and did not increase significantly after TRH administration. We conclude that, in contrast to healthy control dogs, primary hypothyroid dogs respond to TRH administration with a significant increase in the plasma GH concentration, possibly as a result of transdifferentiation of somatotropic pituitary cells to thyrosomatotropes.     

Injection of porcine growth hormone releasing hormone gene plasmid in skeletal muscle increases piglets' growth and whole body protein turnover

The aim of the current study was to investigate the effects of a porcine growth hormone releasing hormone (pGHRH) gene plasmid injection in piglets on growth performance and whole body protein turnover. Sixty male Canadian Landrace × Chinese Taihu piglets were assigned to an intramuscular injection of 0 (control), 0.25, 0.5, 1 and 2 mg. All pigs were fed with the same diet (crude protein: 239.8 g/kg, digestible energy: 14.28 MJ/kg) at ad libitum intake. Protein turnover was determined on the 22nd day with a three-pool model by using a single-dosage, end-product analysis method with ¹⁵ N-glycine as a tracer. Injection of the pGHRH gene plasmid increased the piglets' growth rate, altered feed intake and decreased feed conversion ratio. It increased plasma growth hormone releasing hormone (GHRH), growth hormone (GH), insulin-like growth factor-I (IGF-I) and somatostatin but reduced serum urea and triglyceride. It reduced the urinary nitrogen excretion and led to higher nitrogen retention as well as the efficiencies of nitrogen retention and digestible N utilization. It increased the rates of protein synthesis, protein breakdown and net protein gain. Excretion of endogenous urinary nitrogen was reduced and nitrogen reutilization rate was improved. Conclusions: Injection of the pGHRH gene plasmid in skeletal muscle stimulated GHRH, GH and IGF-I excretion in piglets. Protein deposition was increased by an increase in protein synthesis and a smaller increase in protein breakdown, which was accompanied by reducing amino acid oxidation and increasing nitrogen reutilization.     

Dietary thyroid hormone improves growth and muscle protein accumulation of black-boned chickens

1. The objective of the study was to examine the effect of dietary thyroid hormone on performance and muscle protein accumulation of black-boned chickens. 2. A total of 720 1-d-old birds was housed in 24 pens and assigned to 4 diets containing triiodothyronine (T3) at 0, 0.1, 0.3 or 0.5 mg/kg. 3. The trial was split into starter (0 to 4 weeks) and grower (5 to 8 weeks) phases. At the beginning of the grower phase, each pen was split into two; one subgroup was fed basal diet (T3-) and the other continued with T3-added diet (T3+). 4. Dietary T3 at 0.1 mg/kg improved average daily body weight gain until week 6 but retarded it thereafter. However, T3 at 0.5 mg/kg depressed growth throughout the whole period. During weeks 7 to 8, T3 retarded growth, whereas growth recovered when T3 was withdrawn from the diet. 5. Birds fed the diet containing 0.1 mg/kg during weeks 0 to 4 and those receiving basal diet during weeks 5 to 8 showed the greatest thigh muscle growth, but this growth was depressed when they were fed the 0.5 mg/kg diet during weeks 0 to 8. 6. Serum T3 concentration was increased, while thyroxine (T4) concentration was decreased by dietary T3 treatment at 2 weeks old. At 4 weeks old, T3 and T4 concentrations decreased. At 6 and 8 weeks old, among T3-treated groups the serum T3 concentration of the T3- group was higher than that of the T3+ group. 7. In conclusion, dietary T3 improved weight gain and muscle growth of black-boned chickens before week 6, whereas supplementation depressed growth after 6 weeks. Optimum dietary T3 concentrations showed a carry-over effect on both body weight gain and thigh muscle growth.     

Pathology and residues in veal calves treated experimentally with clenbuterol

Six veal calves were medicated with clenbuterol at 20 μg kg bodyweight⁻¹ day⁻¹ for 42 days before they were slaughtered, to evaluate the lesions and residues in target organs. Compared with six unmedicated calves the most noticeable changes were tracheal dilatation, decreased uterine weight, slight mucous hypersecretion in the uterus and vagina and depletion of liver glycogen. The highest concentrations of clenbuterol (62 to 128 ng/g⁻¹) were recorded in the choroid/retina, and the aqueous humour had the lowest concentration (0·5 to 2·4 ng ml⁻¹). The residue concentrations were higher than the maximum residue level set for clenbuterol (0·5 ng g⁻¹)     

Skeletal deformities associated with nutritional congenital rickets in newborn lambs

Abstract

CASE HISTORY: A group of 545 pregnant rising 2-year-old Coopdale ewes on a Southland sheep farm were grazed over winter on a fodder beet (Beta vulgaris) crop. Subsequently, 45 out of approximately 750 lambs were born with a variety of skeletal deformities, including shortened limbs, varus and valgus angular limb deformities, palmar grade stance and cranial bowing of the carpus. Analysis of the crop showed the fodder beet contained a low percentage of phosphorus. In addition, 60 out of 460 rising 2-year-old ewes that had been grazed on the fodder beet crop as 1-year-olds had incisor abnormalities and malocclusion.

PATHOLOGICAL FINDINGS: Two affected lambs (1-day-old and 3-days-old) with representative clinical signs examined postmortem were found to have markedly enlarged costochondral junctions, and noticeably enlarged long bone metaphyses. In addition, one lamb had a dense band of metaphyseal sclerosis beneath the physes of all long bones examined. Histopathological findings included small islands and columns of chondrocytes and eosinophilic cartilage matrix present in the metaphysis. Metaphyseal trabeculae were disorganised and often lined by accumulations of pale pink osteoid; similar pale pink osteoid was also present in the cortices. Unerupted molar teeth in the affected lambs lacked a layer of enamel, and the dentine was irregular with globular basophilia.

DIAGNOSIS: The gross and histopathological lesions were consistent with a diagnosis of rickets.

CLINICAL RELEVANCE: Nutritional congenital rickets has not been previously diagnosed in sheep, but is a recognised disease of human infants with vitamin D deficient mothers. The rickets in affected lambs was most likely associated with phosphorus deficiency as a result of the pregnant ewes grazing fodder beet during gestation. While vitamin D deficiency was not definitively ruled out in these cases, practitioners are alerted to the possible effects of feeding phosphorus-deficient fodder beet to ewes for long periods during gestation and to 1-year-old sheep during important growth periods.     

Luteinizing hormone and growth hormone secretion in early lactating Spanish beef cows

The episodic release of luteinizing hormone (LH) and growth hormones (GH) was studied in three suckling regimens and two breeds of Spanish suckled cows. Parda de Montaña (PA) cows (n = 21) were assigned to once‐daily, twice‐daily or ad libitum (ADLIB) suckling. Pirenaica (PI) cows (n = 7) were used to evaluate the breed effect in twice‐daily suckling. Coccygeal blood samples were collected twice weekly during lactation to determine the interval from calving to first ovulation through peripheral progesterone. On day 32 ± 3 post‐partum, jugular blood samples were drawn at 15 min intervals during 8 h to analyse circulating LH and GH. The interval to first ovulation was greater in PA cows suckling ADLIB than in restricted suckling treatment (RESTR1), whereas in RESTR2 it did not differ from the other two treatments. There were no differences between PA and PI cows in the interval to first ovulation. RESTR1 cows showed a tendency to have shorter LH peak widths than ADLIB cows. PA cows showed a tendency to have longer LH peak widths than their PI counterparts. There were no differences across treatments or breeds in any of the GH measures of secretion. The LH release was more affected by breed than by suckling frequency, whereas that of GH was not influenced by any of these parameters. The variables that best allowed discrimination between ADLIB and restricted nursing systems were the interval to post‐partum first ovulation, LH peak number and the mean GH concentration.     

Adipose tissue cellularity and muscle growth in young steers fed the beta-adrenergic agonist clenbuterol for 50 days and after 78 days of withdrawal

Angus steers (n = 40; approximate weight = 300 kg) were administered the beta-adrenergic agonist clenbuterol for 50 d (7 mg.hd-1.d-1), followed by a 78-d withdrawal period. Carcass fatness variables did not differ (P greater than .05) between treated and control animals either after 50 d or after 128 d. Weights of the 9-10-11th rib longissimus muscle were 25% larger, and longissimus cross-sectional areas were 28% greater, in clenbuterol-fed steers relative to controls from 0 to 50 d (P less than .05). After withdrawal these measurements increased no further in the treated steers. Marbling scores were decreased (P less than .05) in clenbuterol-fed steers after 50 d of treatment; this effect persisted after 128 d of withdrawal from treatment. Shear force values were increased 19% (P less than .05) by feeding clenbuterol for 50 d and remained greater (P less than .05) in treated animals after 128 d. Subcutaneous adipocytes in clenbuterol-fed steers were smaller (P less than .05) than those of controls after 50 d, and this effect was still apparent after the 78-d withdrawal period. Rates of lipogenesis did not differ (P less than .05) between treated and control animals at any time. Perirenal (p.r.) adipocytes were smaller (P less than .05) in treated animals after 50 d, but this effect disappeared by the end of the experiment. There was no indication of a bimodal distribution of smaller s.c. or p.r. adipocytes in either of the treatment groups. Apparent hyperplasia of s.c. adipocytes occurred in the area of the 9-10-11th rib in both treated (P less than .10) and control animals (P less than .05) from 0 to 50 d on trial. Within treated animals there was a significant increase (P less than .05) in total adipocytes in this depot during the withdrawal period. Although the effects of clenbuterol on muscle growth generally were reversed after 78 d, the effects of the beta-adrenergic agonist on adipose tissue development were more permanent.