Biomedical subjects

C G Scanes

Publications and source records attributed to C G Scanes.

At least 73 records · Page 4Linked to original sources

PubMed1991

Triiodothyronine (T3) inhibition of growth hormone secretion by chicken pituitary cells in vitro.

These studies examined the cellular basis for the inhibitory effects of triiodothyronine (T3) on growth hormone-releasing factor (GRF)-evoked growth hormone (GH) release from chicken anterior pituitary cells in vitro. A primary monolayer culture of anterior pituitaries from 4- to 8-week-old White Leghorn cockerels was performed as previously described by this laboratory. Following a 72-hr preincubation period, cells were washed and incubated (2 hr) with either secretagogues or media alone (control). T3 (20 ng/ml) or vehicle was added to cells during both the preincubation (48-72 hr) and incubation (2 hr period. Triiodothyronine reduced (P less than 0.05) GH release (ng/ml) in response to (1) GRF; (2) the adenylyl cyclase stimulator, forskolin; (3) the cAMP analog and protein kinase A activator, 8-bromo cAMP; and (4) the phorbol ester and protein kinase C activator, phorbol 12-myristate 13-acetate. Triiodothyronine reduced (P less than 0.05) the intracellular content of GH and total GH (released GH and intracellular GH) irrespectively of whether secretagogues were also present. When GH release was expressed as a percentage of total GH [released GH/(intracellular GH + released GH)], percentage GH released in response to GRF, or the protein kinase A, protein kinase C, or calcium pathway activators was not as great in T3-treated versus non-T3-treated cells. These data indicate that T3 inhibits GRF-evoked GH release by reducing the availability of intracellular stores of GH and by also inhibiting second messenger-stimulated GH release pathways.

1-Methyl-3-isobutylxanthine↗

PubMed1991

Possible involvement of adenylyl cyclase-cAMP-protein kinase a pathway in somatostatin inhibition of growth hormone release from chicken pituitary cells.

Somatostatin (SRIF) reduces growth hormone releasing hormone (GRF)-stimulated growth hormone (GH) release from avian and mammalian adenohypophyseal cells. The present studies examined the intracellular mechanisms mediating SRIF inhibition of GRF-stimulated GH release from chicken pituitary cells. Increases (P less than 0.05) in GH release were observed in the presence of (1) GRF; (2) the adenylyl cyclase stimulator, forskolin; (3) a cAMP analog, 8-bromo-cAMP; (4) the phosphodiesterase inhibitor 3-isobutyl-l-methyl-xanthine (IBMX) combined with GRF; (5) a tumor-promoting phorbol ester and protein kinase C activator, phorbol 12-myristate, 13-acetate (PMA); (6) a diacylglycerol analog, 1,2-dioctanoyl-glycerol (DiC8); and (7) a calcium ionophore, A23187, alone and in combination with PMA. Somatostatin (10 ng/ml) reduced the release of GH stimulated by GRF, forskolin, and 8-bromo cAMP and the GRF-provoked release of GH in the presence of IBMX (P less than 0.05). Somatostatin, however, did not influence GH release in the presence of the protein kinase C activators, PMA or DiC8, or the calcium ionophore A23187. These data suggest that SRIF inhibits GRF-provoked GH release by reducing the ability of the cAMP-protein kinase A but not of the calcium or protein kinase C intracellular message pathways to stimulate GH release.

1-Methyl-3-isobutylxanthine↗

PubMed1991

Comparison of lipolytic and antilipolytic activities of lower vertebrate growth hormones on chicken adipose tissue in vitro.

Mammalian and avian growth hormones (GH) (pituitary derived or biosynthetic) exert two effects on chicken adipose tissue explants in vitro. They (i) increase the basal rate of glycerol release a lipolytic effect) and (ii) inhibit glucagon-stimulated glycerol release (an antilipolytic effect). The ability of lower vertebrate GH preparations to exert lipolytic and antilipolytic effects was examined and biological activity was compared to differences in amino-acid residue sequences and to predicted structure. Irrespective of species origin (blue shark, sturgeon, bonito, yellow tail, salmon, bullfrog, sea turtle), all lower vertebrate GH preparations showed very weak (less than 5% the potency of bovine GH), if any, lipolytic activity, but retained strong antilipolytic activity. The present data indicate that the structural requirements for lipolytic and antilipolytic activities of GH differ in chicken adipose tissue. Despite the high sequence homology (88%) between chicken and sea turtle GH, the latter preparation did not stimulate lipolysis. It is suggested that Pro132, conserved only in lipolytically active GH species (human, bovine, and chicken), represents a major determinant of lipolytic activity in chicken adipose tissue. The structural determinants for antilipolytic activity may comprise any or all of residues 3, 17, 64, 108, 109, and 152.

Adipose Tissue↗

PubMed1991

Growth hormone and insulin-like growth factors in poultry growth: required, optimal, or ineffective?

With a continually expanding market for poultry meat products, increased production demands of as much as 50% by the Year 2000 have been predicted. Indications already exist that this magnitude of expansion is not likely to be met by increased production output and genetic selection alone, and that other methods of improving growth performance per bird via exogenous manipulation of the growth process are needed. Studies in mammalian species clearly demonstrate the importance of growth hormone (GH) and its potential for enhancing productivity in domestic mammals. However, the role of GH in growth of poultry appears to be much more complex. Taken collectively, studies to date indicate that significant, positive effects of GH on growth performance of normal, growing poultry are possible. Expression of such effects appear to be largely contingent on the period of posthatch development (late posthatch being more responsive than early), and the pattern of several key metabolic regulatory hormones resulting in response to GH. Such regulatory hormone responses are largely influenced by the pattern or magnitude of exposure (acute versus chronic) to GH in birds. At this time, the available information on the potential for insulin-like growth factors to enhance growth is limited, and further studies are needed before a definitive role for these peptides in growth and development of poultry can be assigned.

Animals↗

PubMed1990

Endocrine-nutrition interactions in birds.

This review will discuss the uses of avian models, particularly the chicken, to examine nutrition-endocrine interactions. The chicken has been employed extensively to examine nutritional effects. The effects of fasting, protein deficiency and calcium deficiency on endocrine status have been the subject of intense investigation in young chicks and adult female chickens. The ratio of circulating concentrations of triiodothyronine (T3) and thyroxine (T4) is substantially changed by fasting or protein deficiency. Similarly, protein deficiency reduces circulating concentrations of insulin-like growth factor I (IGFI) while protein deficiency increases growth hormone (GH). Moreover, protein deficiency increases the sensitivity and responsiveness of adrenocortical cells. The chicken also as advantages for studying diabetes, endocrine pancreatic functioning due to the splenic lobe of the pancreas being predominantly endocrine in nature, and the cellular mechanism of GH on chicken adipose tissue. The adult female chicken with its high calcium requirement is a unique system for examining nutritional effects on reproduction.

Adipose Tissue↗

PubMed1990

Influence of chronic melatonin implantation on circulating levels of catecholamines, growth hormone, thyroid hormones, glucose, and free fatty acids in the pigeon.

Subcutaneous implantation of melatonin pellets (2 mg melatonin + 30 mg beeswax) for a period of 12 weeks, with reinforcement of implants every 2 weeks, caused significant increases in plasma levels of glucose and growth hormone (GH). Plasma levels of thyroxine (T4) were lower and the triiodothyronine (T3)/T4 ratio was higher in the melatonin-treated pigeons. However, melatonin treatment produced no significant effect on plasma levels of free fatty acids (FFA), T3, epinephrine (E), and norepinephrine (NE), although trends (P greater than 0.05) toward slight increases in FFA and T3 and decreases in E and NE were apparent. Since melatonin treatment caused increases in the levels of plasma glucose and GH and not in those of the other substances measured, it is suggested that melatonin enhances carbohydrate metabolism in preference to lipid metabolism in resting pigeons during the day (photophase) when pineal and circulating levels of melatonin are normally lower than during night (scotophase).

Animals↗

PubMed1990

Stimulation of chicken growth hormone release by phorbol esters.

Synergism between thyrotropin-releasing hormone (TRH) and human pancreatic growth hormone-releasing factor (hpGRF) has been shown in a primary (48 hr) culture of chicken adenohypophyseal cells established in this laboratory. The purpose of the present study was to determine if phorbol esters acting alone or in concert with TRH or hpGRF affect chicken GH release. Collagenase-dissociated chicken adenohypophyseal cells were treated (2 hr) with combinations of TRH, hpGRF, phorbol esters (activators of protein kinase C; PKC), and pharmacologic agents that increase cAMP. Phorbol myristate acetate (PMA) or phorbol dibutyrate (PDBu) alone stimulated GH release in a dose-dependent manner; either phorbol ester (10(-6) M) increased GH release from 100 to 390% over the value obtained in the absence of test agents (control). Similarly, hpGRF (10(-9) M), 8 Br-cAMP (10(-3) M), forskolin (10(-6) M), or isobutylmethylxanthine (IBMX, 10(-3) M) alone elevated GH release by at least 60% over the control value. The combined effects of phorbol esters (either PMA or PDBu) and hpGRF, 8 Br-cAMP, or forskolin on GH release were additive. Only one combination, phorbol esters with IBMX, exerted synergistic effects on GH release. No synergy was shown between TRH (1.3 x 10(-9) M) and either phorbol ester. These findings are the first to implicate PKC in chicken GH release in vitro. In addition, these studies, together with previous results, suggest that TRH and hpGRF synergy occurs via a pathway that arises prior to activation of PKC.

1-Methyl-3-isobutylxanthine↗

PubMed1990

Influence of androgens on plasma concentrations of growth hormone in growing castrated and intact chickens.

Castrated chicks implanted with testosterone or 5 alpha-dihydrotestosterone (5 alpha-DHT) had circulating concentrations of the respective androgen similar to or less than in sham-operated chicks. In castrated chicks, 5 alpha-DHT or 19-nortestosterone (19-NorT) inhibited growth as indicated by body weight, while testosterone and 5 beta-dihydrotestosterone (5 beta-DHT) were without effect. In intact male or female chicks, growth was inhibited by either testosterone or 5 alpha-DHT but was unaffected by 5 beta-DHT or estradiol-17 beta. Plasma concentrations of luteinizing hormone (LH) were reduced in castrated chicks receiving implants of either testosterone or 19-NorT. Only the highest dose of 5 alpha-DHT depressed the circulating concentration of LH; lower doses of 5 alpha-DHT being without effect. During the first 6 weeks of growth, plasma concentrations of GH were unaffected by most steroid treatments (5 alpha-DHT, 5 beta-DHT, low doses of testosterone, estradiol-17 beta) in castrated or in intact male or in female chicks. Similarly, 19-NorT did not affect plasma concentrations of GH in castrated chicks. The high dose of testosterone, however, depressed plasma concentrations of GH in castrated chicks between 2 and 6 weeks of age. Between 8 and 12 weeks of age, all steroids tested, except 5 alpha-DHT, were without effect on plasma concentrations of GH. Plasma concentrations of GH were increased in 5 alpha-DHT-treated chickens. This effect was observed irrespective of dose of 5 alpha-DHT or whether the androgen was administered to castrated or to intact male or to female chicks.

Androgens↗

PubMed1990

Phosphorylation of chicken growth hormone.

The possibility that chicken growth hormone (cGH) can be phosphorylated has been examined. Both native and biosynthetic cGH were phosphorylated by cAMP-dependent protein kinase (and gamma -32P-ATP). The extent of phosphorylation was however less than that observed with ovine prolactin. Under the conditions employed, glycosylated cGH was not phosphorylated. Chicken anterior pituitary cells in primary culture were incubated in the presence of 32P-phosphate. Radioactive phosphate was incorporated in vitro into the fraction immunoprecipitable with antisera against cGH. Incorporation was increased with cell number and time of incubation. The presence of GH releasing factor (GRF) increased the release of 32P-phosphate labelled immunoprecipitable GH into the incubation media but not content of immunoprecipitable GH in the cells. The molecular weight of the phosphorylated immunoreactive cGH in the cells corresponded to cGH dimer.

Animals↗

PubMed1990

Influence of catecholamines, prostaglandins and thyroid hormones on growth hormone secretion by chicken pituitary cells in vitro.

In young chickens plasma concentrations of growth hormone (GH) are depressed by prostaglandins (PG) E1 and E2, epinephrine, norepinephrine, alpha 2 and beta agonists or thyroid hormones. A primary culture of chicken adenohypophyseal cells was used to examine the direct effects of these agents at the level of the pituitary as evaluated by GH release in the presence and absence of growth hormone releasing factor (GRF). Following collagenase dispersion and culture (preincubation, 48 hr) cells were exposed (incubation, 2 hr) to test agents, except for thyroid hormones which were added during the preincubation, and incubation period. Growth hormone release was increased (P less than .05) in the presence of PGE1 (10(-8)M by 34%; 10(-7)M by 54%), PGE2 (10(-8)M by 29%; 10(-7)M by 29%), PGF2 alpha (10(-8)M by 28%), and the beta agonist isoproterenol (10(-7)M by 46%). Basal GH release from chicken pituitary cells was not affected by dopamine, norepinephrine, epinephrine, thyroxine (T4), triiodothyronine (T3), or alpha adrenergic agonists. Growth hormone releasing factor stimulated GH release was not affected by the presence of prostaglandins E1, E2 or F2 alpha in the incubation media. However, GRF stimulated GH release was reduced by high doses of catecholamines: dopamine (10(-6)M by 34%), norepinephrine (10(-6)M by 74%), epinephrine (10(-8)M by 47%; 10(-7)M by 41%; 10(-6)M by 89%), and by the alpha 1 adrenergic agonist, phenylephrine (10(-7)M by 52%), the alpha 2 agonist, clonidine (10(-8)M by 34%; 10(-7)M by 83%) and the beta agonist, isoproterenol (10(-7)M by 64%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Participation of tri-iodothyronine and metabolic clearance rate in the inhibition of growth hormone secretion in thyroxine-treated domestic fowl.

Surgical thyroidectomy increases basal and TRH-induced GH concentrations in the peripheral plasma of immature domestic fowl. Replacement therapy with thyroxine (T4; 100 micrograms/kg per day for 7 days, i.m.) suppressed the GH responses to thyroidectomy. Bolus administration of T4 (10 micrograms/kg, i.m.) to thyroidectomized birds promptly lowered the circulating GH concentrations, which remained suppressed for at least 4 h. Chronic (daily injections for 7 days) or acute (one injection) pretreatment of thyroidectomized birds with iopanoic acid (IOP; 40 mg/bird, i.m.) before the bolus administration of T4 attenuated, but did not prevent, inhibition of circulating GH levels by T4. Administration of IOP (40 mg/bird i.m.) 24 h and immediately before the administration of tri-iodothyronine (T3; 3 micrograms/kg, i.m.) or T4 (10 micrograms/kg, i.m.) also failed to suppress thyroidal inhibition of circulating GH concentrations in thyroidectomized birds. Administration of IOP alone had no effect on GH concentrations. Circulating T3 concentrations were not enhanced following the administration of T4 to IOP-treated birds, indicating its inhibition of hepatic monodeiodinase activity. The metabolic clearance rate (MCR) of 125I-labelled chicken GH in the plasma of thyroidectomized fowl was less than that in sham-thyroidectomized birds. Following pretreatment with T4 (100 micrograms/kg per day for 7 days) sham-thyroidectomized and thyroidectomized birds did not differ significantly in their MCR. The GH secretion rate in thyroidectomized birds was similar to that in sham-thyroidectomized birds and in both groups was markedly reduced following pretreatment with T4. These results demonstrate thyroidal inhibition of circulating GH concentrations in fowl.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Effect of beta-adrenergic agonists on lipolysis and lipogenesis by porcine adipose tissue in vitro.

The effects of the beta-adrenergic agonists isoproterenol, cimaterol, ractopamine and clenbuterol on lipolysis (release of glycerol and free fatty acids) and lipogenesis (incorporation of 14C into fatty acids from [14C]glucose) was examined in porcine adipose tissue explants in vitro. Lipolysis was stimulated by isoproterenol, cimaterol or ractopamine but not by clenbuterol. Insulin reduced the lipolytic effects of the beta-adrenergic agonists (isoproterenol, cimaterol and ractopamine). Lipogenesis was inhibited by all beta-adrenergic agonists tested (isoproterenol, cimaterol, ractopamine and clenbuterol). The antilipogenic effect of the beta-adrenergic agonists was reduced by the presence of insulin in the incubation. Although effects of the different beta-adrenergic agonists varied, all had some direct effects that could be expected to reduce adipose accretion. Effects of beta-adrenergic agonists in the pig are due in part to direct effects on adipose tissue.

Adipose Tissue↗

PubMed1990

Lipolytic and antilipolytic effects of human growth hormone, its 20-kilodalton variant, a reduced and carboxymethylated derivative, and human placental lactogen on chicken adipose tissue in vitro.

The lipolytic and antilipolytic effects of human growth hormone (22K-hGH), its 20-kilodalton variant (20K-hGH), a reduced and S-carboxymethylated derivative (RCM-hGH), and human placental lactogen were examined using chicken adipose tissue explants in vitro. Lipolysis, as determined by glycerol release, was stimulated by 22K-hGH (biosynthetic and pituitary derived), 20K-hGH (pituitary derived), and RCM-hGH (modified biosynthetic). These growth hormone preparations also exhibited similar antilipolytic activity (i.e., transient inhibition of glucagon-induced lipolysis). However, unlike human growth hormone, human placental lactogen neither stimulated lipolysis nor inhibited glucagon-stimulated lipolysis. Some augmentation of glucagon-stimulated lipolysis was observed in the presence of human placental lactogen. These results indicate that the disulfide bridges (Cys53----Cys165; Cys182----Cys189) and amino acid residues 32-46 of hGH are not required for lipolytic or antilipolytic activities of human growth hormone on chicken adipose tissue.

Adipose Tissue↗

PubMed1990

Effect of biosynthetic chicken growth hormone on egg production in White Leghorn hens.

Two studies were conducted to determine if injection of recombinant chicken growth hormone (cGH) influences egg production parameters in older laying hens. In both experiments, hens were subjected to consecutive 3-wk periods consisting of 1) a preinjection period, 2) an injection period, and 3) a postinjection period. During the 3-wk injection period, hens were injected once daily with either 5, 50 or 500 micrograms/kg BW of cGH or physiological saline (vehicle) alone (control group). In both experiments, injection of cGH did not affect (P greater than .05) percentage of daily egg production per hen, Haugh units, or BW during the injection period compared with preinjection hens. In Experiment 1, but not Experiment 2, control hens had reduced shell thickness and feed consumption during the injection and postinjection periods when compared with the preinjection controls. These reductions were not observed in hens receiving injections of cGH (all doses).

Aging↗

PubMed1990

In vivo effects of biosynthetic chicken growth hormone in broiler-strain chickens.

Two experiments were conducted to examine the effects of growth hormone (GH) in growing chickens older than broiler age. In experiment 1, 8 week old male (heavy "broiler" type strain) chickens received daily injections of either biosynthetic chicken GH or an implant of biosynthetic bovine GH for 3 weeks. Neither growth rate (daily weight gain) nor the feed:gain ratio was influenced by either preparation of GH. However, an increase in breast muscle was observed in birds receiving the higher dose (250 micrograms/kg/day) of chicken GH. No changes were observed with chicken GH treatment on the weights of the fat pad, heart, gizzard and shank bone or on shank bone length or on plasma concentrations of free fatty acids. Experiment 2 employed 12 week old male, heavy strain, chickens with biosynthetic chicken GH being administered via Alzet osmotic pumps. In this study, GH (50 micrograms/kg/day) increased growth rate, body weight, pectoralis (breast) muscle weight, adipose tissue weight, bursa Fabricius weight and the plasma concentrations of free fatty acids. It is concluded that GH can influence carcass composition and growth in older chickens.

Aging↗

PubMed1989

Growth hormone release from chicken anterior pituitary cells in primary culture: TRH and hpGRF synergy, protein synthesis, and cyclic adenosine 3'5'-monophosphate.

Our earlier work showed that the effects of thyrotropin-releasing hormone (TRH) and human pancreatic growth hormone-releasing factor (hpGRF) on growth hormone (GH) release are synergistic (greater than additive) in a primary culture of chicken adenohypophyseal cells. The purpose of the present studies was to investigate the possible participation of protein synthesis and cyclic adenosine 3'5'-monophosphate (cAMP) in GH release. Following culture (48 hr), cells were incubated for 2 hr with test agents. Cycloheximide (an inhibitor of protein synthesis) had no effect on basal (absence of test agent) GH release or hpGRF-induced GH release. However, cycloheximide abolished the synergy between TRH and hpGRF. Although neither TRH nor hpGRF alone stimulated GH production (intracellular GH plus GH release) during a 2-hr incubation period, in combination these secretagogues increased total GH. These findings suggest that GH release from the chicken somatotroph under conditions of TRH and hpGRF synergy requires protein synthesis. In other studies, cells were exposed to agents inducing the formation of cAMP and either TRH or hpGRF. 8 Br-cAMP (10(-3) M), forskolin (10(-6) M), or isobutylmethylxanthine (IBMX; 10(-3) M) alone stimulated GH release to values between 30 and 50% over the basal value. The combined effects of each of these agents and TRH on GH release were synergistic. Similarly, IBMX and hpGRF exerted synergistic effects on GH release. In contrast, no synergy was shown between hpGRF and either 8 Br-cAMP or forskolin; their combined actions were less than additive.

1-Methyl-3-isobutylxanthine↗

PubMed1989

Somatostatin inhibition of thyrotropin-releasing hormone- and growth hormone-releasing factor-induced growth hormone secretion in young and adult anesthetized chickens.

The present communication examines the influence of somatostatin (SRIF14) on basal and thyrotropin-releasing hormone (TRH)- or growth hormone-releasing factor (GRF)-induced GH secretion in young (6 week old) and adult male chickens. Studies were performed in sodium pentobarbitone-anesthetized chickens where basal plasma concentrations of GH are low and both TRH and GRF consistently stimulate GH release. In both young and adult chickens, basal GH secretion was reduced by SRIF14 infusion (3 micrograms/kg/min). Similarly, in adult and young birds, the GH secretory response to a challenge with a GRF bolus (10 micrograms/kg) was inhibited by the concomitant intravenous infusion of SRIF14 (0.3 or 3.0 micrograms/kg/min). In adult chickens, the GH response to TRH (10 micrograms/kg) was suppressed (by 93%) by SRIF14 infusion (3 micrograms/kg/min) and tended to be inhibited (by 29%) by a lower dose of SRIF14 (0.3 micrograms/kg/min). In contrast, in young chicks, GH release following TRH challenge (either 1 or 10 micrograms/kg) was only partially inhibited by SRIF14 infusion (3 micrograms/kg/min). The response to a TRH challenge (10 micrograms/kg) was unaffected by the low dosage of SRIF14 infusion (0.3 micrograms/kg/min). It is concluded that SRIF14 inhibits both GRF- and TRH-stimulated GH release in young and adult chickens.

Aging↗

PubMed1989

Plasma LH and gonadal LH-binding cells in normal and surgically decapitated chick embryos.

Plasma luteinizing hormone (LH) concentrations and the numerical density (Nv) of gonadal LH-binding (LH-positive) cells were determined in intact male and female chick embryos from Days 10.5 through 18.5 of incubation for plasma LH and from Days 6.5 through 19.5 for LH-binding cells, as well as in Day 15.5 decapitated ("hypophysectomized") embryos with pituitary transplants for both plasma LH and LH-binding cells. The data demonstrate that LH is already present in the plasma of male and female embryos as early as Day 10.5, the first day examined. Plasma LH levels in hypophysectomized embryos were statistically significantly lower than those of intact embryos, while pituitary transplants to the chorioallantoic membrane of hypophysectomized embryos elevated plasma LH concentrations to levels not statistically different from those of intacts. The "role(s)" of plasma LH levels and changes in form and numerical density (Nv) of gonadal LH-binding cells in the maturation of the pituitary-gonadal axes of the chick embryo are discussed and evaluated.

Animals↗