Biomedical subjects

C G Scanes

Publications and source records attributed to C G Scanes.

At least 55 records · Page 3Linked to original sources

PubMed1994

Disappearance rate of glycosylated and non-glycosylated chicken growth hormone: influence on biological activity.

The disappearance rates for glycosylated (GcGH) and non-glycosylated chicken growth hormone (NGcGH) were compared following their intravenous injection into anaesthetized adult laying hens. The metabolic clearance rate of GcGH was about 20% lower (P = 0.13) compared to NGcGH. Similarly, there was a tendency towards a longer half-life for GcGH. No major physiological significance could be attributed to the glycosylation state of the preparations as far as their effects on circulating insulin-like growth factor I and iodohormone levels were concerned.

Analysis of Variance↗

PubMed1994

Influence of adenosine or adrenergic agonists on growth hormone stimulated lipolysis by chicken adipose tissue in vitro.

In vitro lipolysis by chicken adipose explants was stimulated by growth hormone (GH) or glucagon. Adenosine or the adenosine agonist, N6-phenylisopropyladenosine (PIA), inhibited GH stimulated lipolysis, the effect of adenosine not being observed in the presence or adenosine deaminase. Glucagon induced lipolysis was also reduced by PIA. It is suggested that adenosine may act by Gi linked to either adenylate cyclase (for glucagon) or the signal transduction mechanism for GH. Lipolysis was not stimulated by GH in the presence of phenylephrine (alpha 1 adrenergic agonist), isoproterenol (beta adrenergic agonist), adrenaline or glucagon. Although the presence of p-amino clonidine (alpha 2 adrenergic agonist) depressed basal lipolysis, a response to GH was still present. Either glucagon or beta-adrenergic agonists (isoproterenol, adrenaline) stimulated lipolysis. In both cases, GH attenuated the lipolytic response to these hormones, which act via a cyclic adenosine monophosphate signal transduction mechanism.

Adenosine↗

PubMed1994

Triiodothyronine reduces growth hormone secretion and pituitary growth hormone mRNA in the chicken, in vivo and in vitro.

The influence of triiodothyronine (T3) on growth hormone (GH) mRNA and GH secretion has been examined in the chicken. Initially T3 treatment in the diet for three days did not alter plasma concentrations of GH. Plasma concentrations of GH were depressed with seven and 14 days of T3 treatment (1 or 5 ppm in the diet). There was a concomitant decline in pituitary GH mRNA with T3 treatment. Pituitary GH content was reduced with 14 but not seven days of T3 treatment. No effect of T3 was observed on the percentage by somatotroph cells in the anterior pituitary gland by fluorescence flow cytometry analysis. While exposure of pituitary cells in vitro from young chickens to GHRF for 2 hr increased GH mRNA, no effect was observed with T3. The presence of T3, for 48 hr in vitro, tended to reduce GH mRNA in adenohypophyseal cells from young chickens and decreased GH mRNA with anterior pituitary cells from adult chicks. It is concluded that T3 chronic administration of T3 depresses circulating concentrations of GH, at least in part, by decreasing GH mRNA and hence GH synthesis.

Analysis of Variance↗

PubMed1994

Neuroendocrine-immune interactions.

The role of the neuroendocrine system in influencing both immune development and function has become an area of active research within many model systems, including the chicken. It is now clear that the neuroendocrine system can exert immediate feedback regulation on the immune system as well as control specific aspects of immune differentiation and development. The primary lymphoid organs of avian species (i.e., the thymus and the bursa of Fabricius) are also known to function as endocrine organs. These produce hormonal products that influence the development of lymphoid cells and that may feed back on the neuroendocrine system. In conjunction with the endocrine activities of the primary lymphoid organs, immune and accessory cells are known to produce a variety of secreted products or cytokines that have the potential not only for the regulation of immune function but also for mediating neuroendocrine activities. Finally, it has been demonstrated in a variety of species that leukocytes are capable of producing endocrine mediators previously believed to be produced only under the direct control of the hypothalamic-pituitary axis. Thus, there are numerous possibilities for bidirectional interactions between the immune and neuroendocrine systems. This discussion focuses primarily on these interactions with an emphasis on the means by which the hormonal mediators, growth hormone and thyroid hormone, may affect the thymus and the thymic microenvironment. The role of the adrenocorticoids and gonadal steroids in regulating immune function and their involvement in immune feedback circuits are also discussed.

Amino Acid Sequence↗

PubMed1993

Immunocytochemical studies of chicken somatotrophs and somatotroph granules before and after hatching.

Immunocytochemical methods were used to gain information about the embryonic development of chicken somatotrophs before and after hatching. To localize growth hormone, anterior pituitary sections were incubated with growth-hormone antibody, and then an indirect peroxidase method was used for light microscopy and an immunogold method for electron microscopy. The earliest evidence of embryonic somatotrophs was seen at 12 days. At this stage somatotrophs were sparse (0.2% of parenchymal cells) and their granules were pleomorphic with elongated ovoid and lozenge shapes predominating. Few of the immunogold-labeled somatotroph granules of the embryo were spherical until 15 days after fertilization. At 18 days, most of the granules were spherical (their shape in the adult chicken). During the six days between the 15-day-old embryo and the 1-day-old chick, the number of gold particles per granule section approximately doubled suggesting an increase in growth hormone content of the granules. This rise was the result of increases in the size of the granule sections and in the concentration of gold particles in the sections. During the embryonic period of 12-20 days, somatotrophs were not more than 3.6% of the anterior pituitary cell population. During the following two days, between the 20-day-old embryo and the 1-day-old chick, the percentage of somatotrophs in the pituitary parenchymal cell population rose rapidly from 3.6% to 20.7% and then increased slowly to 24.6% during the period of 1-5 days after hatching.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

The concept of metabolic clearance rate in endocrinology. A case study of growth hormone in different lines of meat-type chickens.

Disappearance of growth hormone from blood (plasma) was studied in young broiler chickens in two experiments: a) following single injection of GH (50 micrograms or 250 micrograms/kg) to anesthetized chicks; b) injection of GH (50 micrograms/kg) (under anesthesia) to two lines of broilers selected for either rapid growth or feed efficiency. Clearance of GH never followed a single negative exponential curve. Characterization of the disappearance by a single metabolic clearance rate and half-life time were found to be inaccurate and inappropriate on methodological grounds. High doses of hormone might disturb receptor or catabolism equilibria and result in aberrant values of MCR which could probably be because of the very dynamic nature of the GH clearance system, which appeared to be influenced by dose, line (or genetics of the animal) and by some indices of clearance. Therefore, physiological significance of such data must be interpreted carefully.

Animals↗

PubMed1993

Diurnal-nocturnal changes in food intake, gut storage of ingesta, food transit time and metabolism in growing broiler chickens: a model for temporal control of energy balance.

1. Diurnal-nocturnal changes in food intake, gut storage of ingesta, food transit time and heat production were studied in male broiler chickens reared under a 14L:10D lighting schedule (lights on from 06.00 to 20.00 h). 2. Food consumption during the scotophase was negligible. Peak food consumption during the photoperiod occurred at the beginning of the photoperiod and in the late afternoon. 3. During the photoperiod, the crop and proventriculus/gizzard contained only small quantities of ingesta. However, at the beginning of the scotoperiod, dried ingesta content of crop and proventriculus/gizzard increased by 10.5- and 2.76-fold respectively. This increase was followed by a gradual decrease towards the end of the scotoperiod. 4. Food transit time during the scotoperiod was significantly longer than that during the photoperiod. 5. The daily pattern of heat production closely followed the 14L:10D lighting schedule. Total heat production during darkness averaged 53% of total heat production during the photoperiod. 6. It was estimated that the storage of energy (as ingesta) in the crop and proventriculus/gizzard, followed by its gradual release and the increased food transit time during the night, contributed 75.5% of nocturnal energy needs. It must be recognised that these mechanisms play a major role in the energy balance of the growing chicken during periods without food intake.

Analysis of Variance↗

PubMed1993

Ontogeny of pituitary growth hormone and growth hormone mRNA in the chicken.

The changes in pituitary growth hormone (GH) mRNA levels have been determined by Northern blot analysis and laser densitometry during embryonic development and posthatch growth of white Leghorn cockerels. Pituitary GH mRNA levels were observed to progressively increase between 18 days of embryonic development to a maximum at 4 weeks of age (posthatch). Subsequently, pituitary GH mRNA levels declined between 4 and 8 weeks of age, and between 12 weeks of age and adulthood. Pituitary GH contents showed increases during embryonic development and posthatch growth that paralleled the rise in GH mRNA. The decline in pituitary GH mRNA levels between 4 weeks of age and adulthood occurs when GH secretion has been observed previously to decline.

Aging↗

PubMed1993

A growth hormone (GH) analog that antagonizes the lipolytic effect but retains full insulin-like (antilipolytic) activity of GH.

An analog of bovine growth hormone (bGH-M8: [Leu117, Arg119, Asp122]-bGH) with an idealized amphiphilic third alpha-helix has been proposed to be a functional antagonist of GH. In accordance with this proposition, bGH-M8 profoundly inhibited bGH-stimulated lipolysis by chicken adipose tissue in vitro. bGH-M8 alone was a weak agonist in the lipolytic assay (1.9% the potency of bGH). The present evidence indicates that bGH-M8 is a competitive antagonist of the lipolytic action of GH based upon the following results: (i) increasing concentrations of bGH-M8 (antagonist) produce progressively greater inhibition of GH-stimulated lipolysis; (ii) increasing concentrations of bGH (agonist) are capable of overcoming this antagonism; and (iii) Schild plot analysis (slope = -0.94) suggests a receptor antagonist with an equilibrium dissociation constant (KB) of 4.54 nM. In contrast to the antagonistic effects of bGH-M8 on bGH-stimulated lipolysis, bGH-M8 retained full insulin-like ("antilipolytic") activity (i.e., inhibition of glucagon-induced lipolysis). bGH-M8 and bGH were similarly potent in eliciting antilipolytic effects in vitro. Moreover, the antilipolytic effects of bGH-M8 and bGH were additive. Therefore, the third alpha-helix (particularly residues 117, 119, and 122) of bGH contains major structural determinants for the lipolytic effects of GH. The ability of bGH-M8 to act as an antagonist for at least one action of GH (lipolysis) while being a full agonist for another (antilipolysis) suggests that different domains of GH are responsible for its various biologic activities, possibly involving different binding sites and/or signal transduction mechanisms.

Animals↗

PubMed1992

Lipolytic and diabetogenic effects of native and biosynthetic growth hormone in the chicken: a re-evaluation.

1. There is controversy as to whether growth hormone (GH) is lipolytic and/or diabetogenic in vivo in chickens. The ability of GH to influence circulating concentrations of free fatty acids was examined in anaesthetized (suppressing endogenous GH secretion) adult and young chickens using three preparations of GH. 2. Plasma concentrations of free fatty acids were increased following the intravenous injection of native bovine GH (50 micrograms/kg to either young or adult chickens), recombinant chicken GH (American Cyanamid) (50 micrograms/kg to adult chickens) and recombinant chicken GH (Amgen) (50 micrograms/kg to young chickens). 3. Similarly, infusion of recombinant chicken GH was accompanied by a gradual increase (P less than 0.05, 90 min following start of infusion) in plasma concentrations of free fatty acids in both anaesthetized hypophysectomized and sham operated young chickens. 4. These data support an acute lipolytic role for GH in the chicken. 5. The injection of neither bovine nor chicken GH had any consistent effect on circulating concentrations of glucose. Moreover, if GH was administered in the presence of glucose, GH had no effect on plasma concentrations of glucose. 6. Further evidence for a lack of a diabetogenic role for GH comes from the inability of chronic administration of GH to influence the decline in plasma concentrations of glucose following challenge with the insulin secretagogue, tolabutamide.

Animals↗

PubMed1992

Abdominal adipose tissue from broiler chickens selected for body weight or for food efficiency differ in in vitro lipolytic sensitivity to glucagon and to chicken growth hormone, but not to dibutyryl cAMP.

1. Differences in responses to lipolytic agents have been investigated in vitro in abdominal adipose tissue from lines of broiler chickens selected for body weight (GL, a 'fat' line) or for food efficiency (FC, a 'lean' line). 2. Dibutyryl cyclic adenosine monophosphate stimulated in vitro lipolysis, as measured by the glycerol release, by adipose tissue from GL or from FC chickens to the same extent. 3. Glucagon stimulated glycerol release from adipose tissue from FC chickens, but not from GL chickens. 4. Adipose tissue from GL chickens was much more sensitive to chicken growth hormone (GH) compared to FC chickens. 5. It is concluded that the selection criteria applied influenced the number of adipose GH and glucagon receptors, the number of adipose GH receptors being lower and of glucagon receptors being higher in FC chickens compared to GL chickens.

Abdomen↗

PubMed1992

Phosphorylation of prolactin and growth hormone.

To determine whether GH and prolactin could be phosphorylated, turkey GH, chicken GH, chicken prolactin and turkey prolactin were incubated in vitro with the catalytic subunit of protein kinase A and [gamma-32P]ATP. Phosphorylation was assessed after sodium dodecyl sulphate-polyacrylamide gel electrophoresis, Western blotting and autoradiography. Polyacrylamide electrophoresis showed that both purified native chicken GH and turkey GH were phosphorylated under the conditions employed. However, the glycosylated variant of chicken GH did not appear to be labelled. Chicken prolactin, turkey prolactin and the glycosylated variant of turkey prolactin were all intensely phosphorylated by protein kinase A. Ovine and rat prolactins could also be phosphorylated by protein kinase A. The phosphate content of different native prolactin (turkey, ovine and rat) and GH (ovine and chicken) preparations was also determined and found to be significant. Chicken pituitary cells in primary culture incorporated 32P in GH- and prolactin-like bands isolated by non-denaturing polyacrylamide gel electrophoresis, and this was stimulated by phorbol myristate acetate. Phosphorylation of GH and prolactin may thus explain some of the charge heterogeneity of these hormones.

Animals↗

PubMed1992

Effect of triiodothyronine on the expression of T cell markers and immune function in thyroidectomized White Leghorn chickens.

Hypothyroid K-strain chickens were produced by neonatal thyroidectomy and treatment with 6-propyl-2-thiouracil. Thyroidectomized birds were given 0, 1.5, 4.5, 15, or 45 micrograms/kg body wt of triiodothyronine (T3) by daily injection. At 5 weeks of age, thymocytes were prepared for flow cytometric analysis of CT-1a, CD3, CD4, and CD8 expression. Sham-operated birds had the smallest proportion of CT-1a+ cells and the brightest CT-1a+ cells. Unsupplemented thyroidectomized birds presented an inverse picture, while T3-treated thyroidectomized birds were intermediate. Fewer and less brightly labeled CD3+, CD4+, and CD8+ cells were associated with sham-operated birds or with higher levels of T3 replacement. Low levels (1.5 microgram/kg body wt) or no T3 treatment produced a greater proportion of positive, highly fluorescent cells. The ratios of CD4+ to CD8+ thymocytes were increased (P less than or equal to 0.05) by T3 supplementation. Functionally, thyroidectomy produced a decrease in mitogen-stimulated proliferation of peripheral blood lymphocytes. This effect was ameliorated by T3 supplementation. Further, thyroidectomy produced an elevation of plasma growth hormone concentrations. These results suggest that thyroid factors and alterations of thymic status significantly affect the generation of specific thymus-derived lymphocyte populations and their functional capabilities, perhaps due to changes in the thymic microenvironment. These alterations may have important consequences for the development of immunocompetence and disease resistance in chickens.

Animals↗

PubMed1992

Effect of thyroxine and chicken growth hormone on immune function in autoimmune thyroiditis (obese) strain chicks.

The effect of thyroxine (T4) and/or recombinant chicken growth hormone (rcGH) supplementation on immune function and on immune cell maturation was examined in Obese strain chickens. Day-old Obese strain chicks received the control treatments or were treated with either T4 (supplemented in the diet), T4-rcGH, or rcGH (by daily injection) in a full factorial design. At 4 weeks of age, the proliferative activity of peripheral blood T cells to either mitogenic or allogenic cell (mixed lymphocyte response) challenge was assessed. At the same time, peripheral blood lymphocytes and thymocytes were collected and prepared for flow cytometry analysis. Proliferative responses to both T cell mitogens and allogeneic splenocytes were significantly increased (P less than 0.05) by rcGH treatment, while the combined T4-rcGH treatment resulted in a significant increase in allogeneic and in concanavalin A responsiveness, but not in the response to phytohemagglutinin. All supplemented groups showed a significant decrease in the mean fluorescent intensity for CT-1a+ thymocytes, while thymocytes from birds receiving either T4 or rcGH alone had higher proportions of CD4+ and CD8+ cells. The monoclonal antibody staining of thymocytes from T4-rcGH-supplemented animals more closely resembled that of the unsupplemented controls. Among the peripheral blood lymphocytes, there were no changes in the numbers of CD4+, CD8+, or sIg+ cells as a result of treatment. The mean fluorescent intensity of sIg+ cells was significantly decreased, however, as a result of T4 supplementation when given either alone or in combination with rcGH. Finally, the mean fluorescent intensity ratios of CD4+ to CD8+ cells was significantly increased as a result of rcGH supplementation. These results strongly support a role for both the thyroid hormones and growth hormone in regulating and/or enhancing immune function, with changes in functional responses paralleled by concomitant changes in the T cell populations as expressed by shifts in T cell surface marker expression.

Animals↗

PubMed1992

Inhibition of growth in chickens by testosterone, 5 alpha-dihydrotestosterone, and 19-nortestosterone.

The growth response of poultry to androgens is ambiguous, with both increases and decreases being reported. This may reflect the use of pharmacological doses. The present study examined the effect of physiological concentrations of androgens on growth of intact male, intact female, and castrated chickens. Physiological concentrations of androgen were attained by subcutaneous silastic implants. In mammals, androgens have both androgenic effects on the reproductive organs and anabolic growth-promoting effects on body and muscle growth. Some androgens, for instance 5 alpha-dihydrotestosterone (5 alpha-DHT) have high androgenic activity (5 alpha-DHT greater than testosterone) but others, e.g., 19-nortestosterone, have high anabolic activities (19-nortestosterone greater than testosterone greater than 5 alpha-DHT). The relative effects of testosterone, 5 alpha-DHT, and 19-nortestosterone on growth were compared in chickens. In young, intact male and female chicks, growth was suppressed by 1.0-cm silastic implants of testosterone and 5 alpha-DHT (5 alpha-DHT greater than testosterone). Castrated chicks were implanted with implants of various sizes (.3, 1.0, and 3.0 cm) containing testosterone, 5 alpha-DHT, or 19-nortestosterone. The androgens inhibited body weight gain: 19-nortestosterone reducing body weight at all three doses, 5 alpha-DHT reducing body weight at the intermediate and high doses, and testosterone tending to reduce body weight only at the high dose. Testosterone (3.0 cm), 5 alpha-DHT (all doses), and 19-nortestosterone (all doses) reduces skeletal growth, as indicated by shank-toe length. In contrast to their growth-suppressing effect, all three steroids exerted an androgenic effect; stimulating comb and wattle development (19-nortestosterone greater than 5 alpha-DHT greater than testosterone). It is concluded that androgens are androgenic but are not anabolic in chickens.

Adipose Tissue↗

PubMed1992

Effects of androgen (testosterone, 5 alpha-dihydrotestosterone, 19-nortestosterone) administration on growth in turkeys.

The present studies examined the effect of three androgens, testosterone, a reduced form 5 alpha-dihydrotestosterone (5 alpha-DHT), and the readily aromatizable anabolic androgen, 19-nortestosterone, on growth in male and female turkeys. Growth (body weight, average daily gain, and right breast muscle weight) was increased by testosterone (females), 5 alpha-DHT (males and females), and 19-nortestosterone (males and females). Moreover, both feed:gain ratio and the weight of abdominal adipose tissue was reduced in turkeys treated with testosterone (females), 5 alpha-DHT (males and females), and 19-nortestosterone (females and males). Bursa of Fabricius weights were reduced in androgen-treated male or female turkeys with the decrease following 19-nortestosterone being greater than those observed with either testosterone or 5 alpha-DHT. Androgen treatment had no effect on skeletal growth (as indicated by shank-toe length) or weights of the liver, spleen, or testes. In female turkeys, plasma concentrations of hormones were determined following androgen treatment. No effects were observed on plasma concentrations of insulin-like growth factor-I or luteinizing hormone after any androgen treatment. Testosterone administration was followed by a physiological increase in the plasma concentrations of testosterone. Plasma concentrations of growth hormone were unaffected by either 5 alpha-DHT or 19-nortestosterone but reduced by the high dose of testosterone. The effect of castration on growth in the presence or absence of 19-nortestosterone was also examined. Castration did not depress growth compared with sham-operated controls, but increased adiposity. 19-Nortestosterone increased growth of castrated turkeys, increased muscle weight, and reduced abdominal adipose tissue weight.

Adipose Tissue↗

PubMed1992

Evolution of the growth hormone-releasing factor (GRF) family of peptides.

1. The primordial GRF may have arisen quite early in evolutionary history, at or prior to (i.e. should immunoreactivity data be confirmed in invertebrates) the appearance of jawed vertebrates (Gnathostomates). A common evolutionary pathway using gene duplication may have been utilized to generate the GRF super-family of peptides. As most members of this peptide superfamily are produced in the gastrointestinal tract, the question is posed whether the GRF may have similar origins. 2. It is suggested that the GRF superfamily has two major branches: a) GRF; PRP/PACAP; VIP/PHI; secretin and b) Glucagon/GLP-1/GLP-2. GIP is likely to be a member of the glucagon branch. The two branches may be attributable to gene duplication encoding an ancestral molecule. These gene duplications are likely to have occurred prior to the evolution of vertebrates (conservatively 400-500 million years ago, and possibly 1 billion years ago). It is probable that peptides homologous to GRF, VIP and glucagon will be isolated from invertebrates. These invertebrate sequences will shed further light upon the evolution of this peptide superfamily. 3. Throughout the GRF superfamily, amphiphilic alpha-helical secondary structures represent preferred bioactive conformations. It is assumed that stable, ordered secondary structures conferring enhanced ligand-receptor interactions were conserved due to selective pressures. 4. It is well documented that hypothalamic GRF stimulates adenohypophyseal GH secretion in a variety of species. Thus far, the physiological effects of GRF have been attributed thus to the elevation of GH, and possibly also IGF-I. Recent data suggests a more liberal view; that GRF may also have direct actions in fetal/placental development, reproduction and immune function. Furthermore these direct effects may be mediated via GRF from either hypothalamic or extrahypothalamic (e.g. placenta, testes, ovary, leukocyte) sources. In conclusion, a great wealth of information has accumulated since the discovery of GRF. Examination of the GRF peptide superfamily from an evolutionary perspective has revealed new insights into the synthesis, processing, degradation, conformation and activities of these molecules. Knowledge obtained from these evolutionary comparisons has also become particularly useful in contemporary peptide drug design, which may be liberally viewed as a form of 'artificial evolution' (i.e. the selective pressure being clinical/veterinary requirements for more potent, long-acting GRF analogs).

Amino Acid Sequence↗

PubMed1992

Effects of surgical decapitation and chicken growth hormone (cGH) replacement therapy on chick embryo growth.

The effects of decapitation and chicken growth hormone (cGH) replacement therapy on chick embryo growth has been investigated. Removal of the prosencephalon at 33-38 hrs (1.38 to 1.58 Days) of incubation decreased body (torso) and liver weights as well as skeletal growth as indicated by tibial length. A single pituitary gland transplanted onto the chorioallantoic membrane (CAM) partially restored torso growth and completely reversed the increase in body water content which characterizes decapitated embryos. Replacement therapy with cGH did not influence body weight but did, on Day 16.5 of incubation, increase tibial length and liver DNA content and concentration. These latter findings suggest that there may be limited hypothalamoadenohypophyseal (GH) axis function in the chick embryo. The effects of decapitation on torso growth are also discussed in conjunction with decapitation effects on albumen swallowing (absorption) and yolk absorption.

Albumins↗