Dissertations / Theses: 'Growth hormone'

1

陳蒓 and Tzun Rachel Chan. "Growth hormone therapy for growth hormone deficiency." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31970308.

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Chan, Tzun Rachel. "Growth hormone therapy for growth hormone deficiency." Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22926288.

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3

Holmes, Sarah Jane. "Growth hormone replacement in adults with growth hormone deficiency." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.297239.

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Mahajan, Tripti. "Diagnosis of growth hormone deficiency and study of the effects of growth hormone treatment in growth hormone deficient adults." Thesis, University of Bristol, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.247557.

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5

Ehrnborg, Christer. "Growth hormone in athletes /." Göteborg : Department of Internal Medicine, Institute of Medicine, The Sahlgrenska Academy at Göteborg University, 2007. http://hdl.handle.net/2077/4709.

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6

Van, Koesveld Marika J. "Potential applications of growth hormone-releasing peptide-6 as a growth promotant." Thesis, The University of Sydney, 2003. https://hdl.handle.net/2123/28158.

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Consumer demand for high quality, lean meat has driven pork producers to seek new methods to maximise lean meat production and minimise fat deposition. Manipulation of the somatotropic axis of an animal has been identified as an effective method to increase growth efficiency and decrease adipose tissue deposition. The potential of H-His-D-Trp-Ala-Trp-D-Phe—Lys-NHZ (GHRP-6) to improve grth was evaluated by two methods, as a neonatal imprinting agent, and as an orally active in—feed additive via conjugation to vitamin B12. Neonatal imprinting with once-daily injections of GHRP-6 to piglets for three days postnatally resulted in an 8% increase in slaughter weight when animals were fed a high protein specification diet, compared to control animals fed a standard commercial diet. The increase in growth rate appears to be due to stimulation of feed intake, although the exact mechanism causing this effect is unknown at this stage. Feed efficiency and carcass composition did not differ from control animals. Further refinement of this technology may make it a highly desirable and cost-effective method to enhance growth rate and allow animals to attain a marketable liveweight in a shorter period of time.

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Gleeson, Helena. "Understanding growth hormone sensitivity and responsiveness: factors affecting IGF-1 response to growth hormone." Thesis, University of Manchester, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493445.

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In endocrinology dynamic testing forms an essential part of investigation. To assess the central capacity of the GH-lGF-1 axis there is extensive experience in paediatric and adult populations of numerous physiological and pharmacological tests. However tests to assess the peripheral capacity of the GH-IGF-1 axis beyond a simple baseline lGF-1 level are limited to the IGF-1 generation test (IGFGT).

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Betley, Stephen. "Regulation of hepatocyte function by insulin, growth hormone and thyroid hormones." Thesis, University of Newcastle Upon Tyne, 1991. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287415.

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9

Johnson, Christopher Derek Martin. "Growth hormone in chick embryogenesis." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ28952.pdf.

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10

Edén, Engström Britt. "Growth Hormone and Gender. Studies in Healthy Adults and in Patients with Growth Hormone Disorders." Doctoral thesis, Uppsala universitet, Institutionen för medicinska vetenskaper, 2001. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-1262.

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The use of a new, more sensitive immunoassay for growth hormone (GH) revealed that the serum levels in men were lower than expected in sera drawn ambulatory in the morning after an overnight fast and that the gender difference was more than 10 times greater than reported. These observations led to a more thorough study on the impact of gender and sex steroids on the levels of GH and other hormones in ambulatory morning samples and over a 24-hour period. Furthermore, the impact of gender was studied in GH deficient (GHD) patients and healthy young adults treated with GH, and in patients with acromegaly treated with octreotide. An 80-fold gender difference in the morning GH levels was observed in young individuals as a reaction to ambulation, with decreased levels in men and increased in women. Oral contraceptives (OCs) given to women further increased the morning GH levels. During the day, higher outputs of epinephrine and lower levels of GH were seen in the men, while no gender differences were seen at night. The gender difference in morning GH levels decreased with age due to opposite changes in men and women. Administration of 17β-estradiol (E2) via subcutaneous implants in postmenopausal women, which increased the E2-concentrations to luteal phase levels, had no effect on the morning GH levels, indicating that the different reactions to ambulation do not appear to result from a direct sex steroid effect alone. Short-term administration of GH to young, healthy adults resulted in larger effects on insulin-like growth factor I (IGF-I) and other key metabolic parameters in men than in women. The smallest response was noted in women taking OCs. The clinical studies involving long-term GH treatment of patients with GHD demonstrate a gender difference in GH responsiveness, with women being less sensitive than men, a fact which should have a therapeutic impact in patients with GH disorders. A further gender difference of therapeutic importance was observed in men and women with acromegaly. Long-term treatment with a slow-release formulation of octreotide resulted in higher IGF-I levels in the men, despite equal doses of the drug and similar levels of GH.

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Edén, Engström Britt. "Growth hormone and gender : studies in healthy adults and in patients with growth hormone disorders /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2001. http://publications.uu.se/theses/91-554-4967-0/.

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Harding, Ruth Linda Paulina. "Characterization and purification of receptors for growth hormone in normal and growth hormone-treated ruminants." Thesis, University of Sussex, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.235532.

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Lundberg, Elena. "Growth hormone responsiveness in children : results from Swedish multicenter clinical trials of growth hormone treatment." Doctoral thesis, Umeå universitet, Pediatrik, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-134569.

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The general aims of the thesis were to study GH responsiveness by estimation of pharmacokinetics and bioavailability of injected recombinant human GH (rhGH), of growth response as gain in heightSDS during childhood and puberty, and IGF-I response as change in circulating IGF-ISDS and IGFBP3SDS. Methods Short children were recruited during 1988–1999 into two national randomized multicentre clinical trials on growth until adult height. A group of 117 GHD patients who had been treated from prepuberty with a single GH dose of 33μg/kg/day for at least 1 year were randomized at onset of puberty either to remain on this dose regimen or to an increased dose, GH67μg/kg/day, administered once daily or divided into two doses, GH33x2μg/kg/day. Data on IGF-ISDS and IGF binding protein 3 (IGFBP3)SDS were available from 111 patients and analysed as stated below. The 151 short prepubertal non-GHD patients were randomized into three groups: untreated controls, GH33 or GH67μg/kg/day. A subpopulation from both trials, 128 patients examined annually in Gothenburg, formed the study sample on GH uptake. They received sc GH injections to obtain 16–24 hour GH curves and the GH pharmacokinetics and bioavailability was calculated. Results: A dose-dependent effect on Cmax was found with great intra- and inter-individual variability. Of the Cmax variability, 43% was explained by the rhGH dose and proxies for injection depth. Median bioavailability of the injected dose was 71%, with great variation, mainly dependent on injection depth. In the IGHD group a dose-dependent difference in pubertal gain in heightSDS was found, with mean of 0.8 for the GH67 group and 0.4 for GH33, p<0.01. The mean total gain in heightSDS during treatment was 1.9 for GH67 and 1.4 for GH33, p<0.01. A dose-dependent pubertal ΔIGF-ISDS was 0.5 vs −0.1, p=0.007, correlating to pubertal gain in heightSDS, p=0.003; and was the most important variable to explain the variation in pubertal gain in heightSDS. In the non-GHD group the ΔIGF-ISDS from baseline to mean study level was dose-dependent 2.07 vs 1.20, p=0.001; and correlated negatively with baseline values of IGF-ISDS, rho= -0.56 for GH67, p=0.001, vs rho= -0.82 for GH33, p=0.0001, and correlated positively with gain in heightSDS in both GH-treated groups, rho= 0.42, p<0.001. In multivariable regression analyses, ΔIGF-ISDS was always an important explanatory variable for long-term growth response from the prepubertal period until adult height, while the IGF-ISDS study level per se was not. Conclusion: Growth response to GH treatment was dose dependent with great variability between patients. More pubertal growth was attained by an increased rhGH dose, mimicking the physiology of healthy children, in whom GH secretion rate increases during puberty. This resulted in a gain in IGF-ISDS closely correlating to pubertal gain in heightSDS in both IGHD and non-GHD patients. A broad range in GH responsiveness was found for both growth and IGF response in both diagnostic groups, but lower in the non-GHD group. Higher uptake of a given GH dose was observed after a deep injection and a higher GH concentration. These results are clinically applicable for individuals who remain short close to onset of puberty; by identifying and deeply injecting a rhGH dose that accounts for individual responsiveness, we can stimulate an increment in IGF-ISDS that correlates to gain in heightSDS during puberty.

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Feng, Xiaopeng. "Chicken growth hormone receptor and growth hormone, search for genetic variants which affect commercially important traits." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0026/NQ29933.pdf.

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Feng, Xiaopeng. "Chicken growth hormone receptor and growth hormone : search for genetic variants which affect commercially important traits." Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=42028.

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Chicken genomic DNA containing 5 kb of the 5$ sp prime$ end of the growth hormone (GH) receptor gene and 12 kb of the region up-stream was cloned and a restriction map was constructed. Using subcloned fragments as probes, a HindIII polymorphism was detected in both egg layer and in meat-type chickens. This polymorphic site was mapped at 7 kb up-stream of the coding region of the GH-receptor gene and a PCR assay for the polymorphism was developed to facilitate genotyping of large numbers of chickens.
Alleles of the GH-receptor gene and the GH gene were analyzed for association with traits in chicken strains of different genetic origins. In egg layers, association was significant for juvenile body weight, egg weight, feed consumption and feed efficiency for egg mass (P $<$ 0.05). In meat-type chickens, the GH-receptor allele associated with high juvenile body weight in egg layers was co-selected with leanness. A comparison of the genotype classes revealed that for several traits there was significant interaction between the GH and GH-receptor genotype. The results indicated that there are variants of the genes of the GH-axis which affect traits in White Leghorns and that the effect of a genetic variation in one gene may depend on the variation in another gene.

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Turner, Joel P. "In vivo evidence that preexposure to somatostatin enhances growth hormone responsiveness to growth hormone-releasing factor." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22820.

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The ultradian rhythm of growth hormone (GH) secretion from the anterior pituitary gland is ultimately controlled by the complex interaction of two hypothalamic hormones, a stimulatory GH-releasing factor (GRF), and an inhibitory hormone, somatostatin (SRIF).
In the present study, we used the long-acting SRIF analog, octreotide, as a probe in both the normal and mutant dwarf rat to (1) further clarify the temporal nature of the SRIF/GRF interplay in GH regulation in vivo, and (2) define possible mechanisms of action of SRIF in generating the ultradian rhythm of GH secretion characteristic of the normal male rat. Administration of octreotide to free-moving, chronically cannulated adult male rats resulted in an almost complete obliteration of spontaneous GH pulses for 3 hours, with gradual recovery observed 3-6 hours after injection. Rats pretreated with octreotide i.v. and subsequently challenged with GRF exhibited reduced GH responsiveness to exogenous GRF at 1 hour post treatment. In contrast, preexposure to octreotide for 3 hours resulted in a 2-3 fold enhancement in GH responsiveness to GRF compared to controls pretreated with normal saline to normal saline-pretreated controls. In contrast, we report that preexposure to octreotide (n = 6) in a strain of dwarf rats, which shows a selective reduction in pituitary GH synthesis and storage, failed to significantly enhance GRF-induced GH release.
Our findings suggest that SRIF pretreatment promotes the accumulation of pituitary GH stores in a readily releasable pool so that subsequent GRF challenges can exert an accentuated effect on pituitary somatotrophs. (Abstract shortened by UMI.)

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Pagano, Christopher. "Role of the truncated form of the human growth hormone receptor in regulating growth hormone effects." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114445.

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The binding of human Growth Hormone (GH) to its receptor (GHR) on target cells leads to activation of three major intracellular signaling pathways: JAK2/STAT5, PI3K/AKT and ERK/MAPK. However, in addition to the full length (FL) GHR, there exist two truncated (Tr) GHR isoforms, GHR1-279 and GHR1-277, that lack the majority of their intracellular domain as a result of alternative splicing of GHR mRNA. While both in vitro and in vivo studies suggest that the Tr GHR isoforms have a dominant negative effect on FL GHR by forming stable heterodimers, little is known about their normal physiological functions and their effects on the three major GH signaling pathways. We hypothesized that Tr GHR isoforms play a functionally significant role in human cells and tissues, fine-tuning the ability of GH to activate intracellular signaling and, thus, its biological effectiveness. In HEK293 cells, GH stimulation resulted in rapid and transient effects on pSTAT5b, pAKT and pERK1. Increasing the Tr/FL GHR ratios by transient transfection of a Tr GHR1-279 expression vector resulted in a significant dose-related inhibition of GH's ability to phosphorylate STAT5b, but with no significant inhibition of its ability to phosphorylate AKT and ERK1.These data suggest that Tr GHR can limit the target cell's STAT5b signaling in response to GH, while there is likely an alternative mechanism through which GH is able to activate AKT and ERK. This reveals a possible physiological role for Tr GHR in modulating GH's biological activity differentially in its target tissues.
La liaison de l'Hormone de Croissance humaine (GH) à son récepteur (GHR) sur les cellules cibles conduit à l'activation de trois voies de signalisation intracellulaires majeures: JAK2/STAT5, PI3K/AKT et ERK/MAPK. Cependant, en plus de la forme intégrale (FL) du GHR, il existe deux isoformes tronquées (Tr) du GHR, GHR1-279 et GHR1-277 qui ont perdu la majorité de leur domaine intracellulaire dû à l'épissage alternatif de l'ARNm du GHR. Alors que les études in vitro et in vivo suggèrent que les isoformes tronqués du GHR auraient un effet de dominant négatif sur le GHR FL en formant des hétérodimères stables, peu d'éléments sont connus au niveau de leurs fonctions physiologiques normales et de leurs effets sur les trois voies de signalisation majeure de GH. Nous avons émis l'hypothèse que les isoformes de GHR Tr auraient un rôle fonctionnel significatif dans les cellules et les tissus humains, en régulant de façon précise la capacité de GH à activer la signalisation intracellulaire et donc son efficacité biologique. Dans les cellules HEK293, la stimulation par GH a conduit à des effets rapides et transitoires sur pSTAT5b, pAKT and pERK1. L'augmentation des ratios Tr/FL du GHR par transfection transitoire du vecteur exprimant le GHR1-279 Tr a résulté en une inhibition significative et dépendante de la dose sur la capacité de GH à phosphoryler STAT5b, mais cependant sans inhibition significative sur sa capacité à phosphoryler AKT et ERK1. Ces données suggèrent que le GHR Tr peut limiter la signalisation par STAT5b dans la cellule cible en réponse à GH, tandis qu'il existerait probablement un mécanisme alternatif par lequel GH serait capable d'activer AKT et ERK. Cela révèle un possible rôle physiologique pour le GHR Tr dans la modulation de l'activité biologique de GH de façon différentielle dans ses tissus cibles.

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Zhao, Lidan. "Mechanisms of growth hormone inhibition of adipose tissue growth." Diss., Virginia Tech, 2013. http://hdl.handle.net/10919/49588.

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Growth hormone (GH) is a poly-peptide hormone produced by the anterior pituitary. Growth hormone not only stimulates body and muscle growth but also inhibits adipose tissue growth. The overall objective of this study was to determine the mechanisms by which GH inhibits adipose tissue growth. Three studies were conducted to achieve this objective. The first study was conducted to determine if GH inhibits fat tissue growth by stimulating lipolysis. In this study, adipose tissue weight and adipocyte size were compared between GH-deficient growth hormone releasing hormone receptor (Ghrhr) homozygous mutant mice (i.e., lit/lit mice), lit/+ mice, and lit/lit mice injected with GH. lit/lit mice had less body weight but more subcutaneous fat and larger adipocytes compared to lit/+ mice at the same ages. GH treatment to lit/lit mice for four weeks partially reversed these differences. These data suggest that GH inhibits adipose tissue growth in mice at least in part by stimulating lipolysis. Additional data from this study suggest that GH indirectly stimulates lipolysis in vivo and this indirect mechanism is independent of " adrenergic receptors in the adipose tissue. The second study was conducted to investigate if GH inhibits fat tissue growth also by inhibiting adipogenesis. In this study, stromal vascular fraction (SVF) cells were isolated from subcutaneous fat of lit/+ and lit/lit mice and were induced to differentiate into adipocytes in vitro. Oil Red O staining and gene expression analysis revealed that the SVF cells from lit/lit mice had greater adipogenic potential than from lit/+ mice. This suggests that GH inhibits adipose tissue growth also through inhibition of adipogenesis. Additional data from this study suggest that GH may inhibit adipogenesis by inhibiting the formation of adipogenic precursor cells in adipose tissue in mice. The third study was conducted to determine the role of the central component of GH receptor signaling, STAT5, in GH inhibition of differentiation of bovine preadipocytes. In this study, preadipocytes were isolated from subcutaneous fat of adult cattle and were induced to differentiate with or without GH. Based on Oil Red O staining, gene expression, glycerol-3-phosphate dehydrogenase (G3PDH) activity and acetate incorporation assays, GH inhibited differentiation of bovine preadipocytes into adipocytes. GH induced phosphorylation of STAT5 in differentiating bovine preadipocytes. Overexpression of constitutively active STAT5 through adenovirus mimicked the effect of GH on differentiation of bovine preadipocytes. These data support a role of STAT5 in mediating the inhibitory effect of GH on differentiation of bovine preadipocytes into adipocytes. Overall, GH inhibits adipose tissue by both stimulating lipolysis and inhibiting adipogenesis; GH stimulates lipolysis through an indirect mechanism that is independent of the " adrenergic receptors; GH inhibits adipogenesis through a direct mechanism that may involve the transcription factor STAT5.
Ph. D.

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Dickey, Lindsey Ann. "Peripheral Hormone Interactions with the Growth Hormone-Insulin-Like Growth Factor (GH-IGF) System in Rainbow Trout." Diss., North Dakota State University, 2019. https://hdl.handle.net/10365/31353.

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The growth of vertebrates is primarily regulated by the growth hormone-insulin-like growth factor (GH-IGF) system, but not in isolation. The central question of this dissertation was how do other hormones peripheral to the GH-IGF system interact with the system, including feedbacks by GH and IGF themselves on various tissues in rainbow trout (Oncorhynchus mykiss)? The representative hormones selected were thyroxine, cortisol, and the sex steroids testosterone and estrogen, along with GH and IGF. These hormones were chosen because they are known to affect overall growth and development during specific life events, but exactly what target genes and what mechanisms are involved are only at the early stages of being delineated in fish. Liver and gill tissues were selected as representative tissues to assess the in vitro effects on growth-related genes of the GH-IGF system. A total of more than thirty experiments were conducted, including time- and concentration-response, inhibitory studies, hormone combination studies, and radio-receptor binding assays. Hormones were applied to whole tissue cultures and real-time quantitative-PCR was used to measure hormonal effects on GHR, IGF, and IGFR1 genes. Microsomal preparations were treated with selected hormones and radio-labeled GH or IGF. A gamma counter was used to measure receptor-ligand activity. GH and IGF were found to possess autocrine and/or paracrine actions in self-regulating target growth genes. Thyroxine had no direct effects on targeted growth genes but may interact with other molecules or hormones to elicit its effects on growth and development. Cortisol directly influenced target growth genes in a tissue-specific and isoform-specific manner. Finally, sex steroids differentially regulated the growth genes: estradiol inhibited growth genes while testosterone directly stimulated growth genes. These findings contribute to understanding how hormones peripheral to the GH-IGF system interact with the growth system.
National Science Foundation grant IOS 0920116 to Dr. Mark Sheridan

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Woods, Kathryn Anne. "Molecular mechanisms in growth hormone insensitivity." Thesis, Queen Mary, University of London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391608.

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Walock, Chad Napoleon. "The Discovery of a Novel Growth Hormone Receptor and the Nutritional Regulation of the Growth Related Actions of Growth Hormone." Diss., North Dakota State University, 2017. https://hdl.handle.net/10365/27453.

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The growth hormone (GH) family peptides such as GH, prolactin (PRL), and somatolactin (SL) regulate a wide array of physiological actions including but not limited to growth, metabolism, osmoregulation, and lipolysis. These actions are regulated by many factors both internal and external. I used rainbow trout (Oncorhynchus mykiss) as a model organism to study the effects of GH-family peptides, nutritional state, and serum on insulin-like growth factor (IGF) and growth hormone receptor (GHR) expression. Gene sequencing and phylogenic analysis was applied to characterize a novel GHR. Real-time quantitative-PCR was used to determine IGF and GHR expression levels in liver, muscle, and adipose tissue. Western blotting and pharmacological inhibitors were used to determine signaling pathways. A novel GHR was characterized and determined to be a type 1 GHR with a diverse distribution. It was found to have many features conserved in other GHRs including binding regions, a Y/FGEFS motif, cysteine residues, and N-glycosylation sites. Fasting was shown to decrease GHR1 expression in the liver, adipose tissue and red muscle. GH and PRL were shown to stimulate IGF expression through the ERK, PI3K/Akt, and JAK-STAT signaling pathways. GH-stimulated IGF expression was dependent on nutritional state, as GH was only able to stimulate IGF expression in fed fish. Nutritional state has no direct effect on GH-stimulated GHR expression. Serum was determined to be the mediator of the change in GH sensitivity as pre-treatment with serum from cells of an opposite nutritional state caused cells to react like the opposite nutritional state in GH-stimulated IGF expression. These findings contribute to the understanding of the actions of GH-family peptides and the mechanisms through which GH conducts its diverse actions in times of differing nutritional availability.
National Science Foundation grant IOS 0920116 to M. A. Sheridan

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Kumarnsit, Ekkasit. "Hypothalamic actions of growth hormone secretagogues." Thesis, University of Edinburgh, 2003. http://hdl.handle.net/1842/24795.

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In this study, the rat hypothalamic brain areas; the arcuate nucleus and the ventromedial hypothalamic nucleus, were selected for study of GHRP-6 and L-144,446 effects in vitro. Extracellular recordings showed that electrical activity of neuronal population in the arcuate nucleus was significantly excited by GHRP-6 and L-144,446. Patterns of excitation by either GHRP-6 or L-144,446 were closely similar. The increase in firing rate was observed with latency period of approximately 2 to 5 min. The excitation was sustained for more than 1 h after the secretagogue washout. Interestingly, GHRF-6 was also observed to increase the firing activity of neurones in the ventromedial hypothalamic nucleus. Patterns of increase in firing activity of ventromedial hypothalamic neurones were very similar to those observed in arcuate neurones. This is surprising, because in in vivo studies, Fos protein induction by systemic administration of secretagogues was consistently observed in the arcuate nucleus but not in the ventromedial hypothalamic nucleus. According to our evidence that ventromedial hypothalamic neurones were significantly excited to GHRP-6 in vitro, it was hypothesised that, in vivo, GHRP-6 stimulates neurones in the arcuate nucleus or other nuclei nearby which project their nerve endings to inhibit ventromedial hypothalamic neurones. The majority of neurones in the arcuate nucleus and the ventromedial hypothalamic nucleus that were excited by either L-144,446 or GHRP-6, were significantly inhibited by neuropeptide Y (NPY). Especially in the ventromedial hypothalamic nucleus, 68~% of GHRP-6-excited neurones, compared to 40% of those in the arcuate nucleus, were clearly inhibited by NPY, NPY is a potent orexigenic agent that was previously found to be produced in many neurones in the ventromedial arcuate nucleus. In addition, the existence of a NPY pathway that originates in the arcuate nucleus and projects to the ventromedial hypothalamic nucleus has previously been demonstrated. These results suggest that, in vivo, secretagogues may stimulate NPY neurones in the arcuate nucleus which project their nerve endings to inhibit a sub-population of the ventromedial hypothalamic nucleus. To investigate the mechanism of GHRP-6 action, immunohistochemistry technique was used to detect the induction of Fos, a protein product of the immediate early gene c-fos a protein product of the immediate early gene c-fos, in the accurate nucleus. The results showed that intravenous injection of GHRP-6 significantly increased immunostaining of Fos in the arcuate nucleus. Pretreatment with intravenous administration of NPY caused 61% reduction of number of Fos-positive neurones in the arcuate nucleus induced by GHRP-6. This findings confirm the effects of GHRP-6 on the electrical activity of the arcuate nucleus and support the idea that this brain area is a central site of action of GHRP-6. This thesis describes site of action of secretagogues in the hypothalamus with in vitro and in vivo data. It also shows the functional involvement of NPY in effects of secretagogues on firing activity and induction of Fos protein in this area.

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Dickson, Suzanne Lee. "Neural control of growth hormone secretion." Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283947.

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McGuiness, Lindsay. "Transgenes targeted to growth hormone cells." Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405167.

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Whitehead, Helen Marie. "Growth hormone deficiency in adult life." Thesis, Queen's University Belfast, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.335313.

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Maniou, Zoitsa. "Molecular evolution of pituitary growth hormone." Thesis, University of Sussex, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270719.

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Deng, Luqin. "Determinants of growth hormone receptor downregulation." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009p/deng.pdf.

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Stokes, Keith. "Human growth hormone responses to sprinting." Thesis, Loughborough University, 2001. https://dspace.lboro.ac.uk/2134/34383.

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A number of studies have shown exercise to stimulate human growth hormone (hGH) secretion, although most of these have considered prolonged submaximal or resistance exercise. Only a few have studied maximal sprint exercise, and these studies have demonstrated considerably elevated circulating hGH concentrations during recovery. However, there is little agreement in the literature regarding the regulation of hGH secretion during and after exercise. This thesis describes a series of experiments considering the hGH response to sprint exercise, with the intention of gaining a better understanding of some of the mechanisms involved in regulating the exercise-induced hGH release.

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Villar, David. "Hormonal regulation of the fibre growth and moult cycle in cashmere goats." Thesis, University of Aberdeen, 1998. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU106170.

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The role of selected hormones in the control of hair follicle activity, fibre growth and moult in cashmere goats was investigated by manipulation of prolactin (PRL), thyroid hormones, and growth hormone (GH) individually or in combination. In experiment 1, the effect of different doses of the anti-thyroid drug "propylthiouracil" (PTU), on thyroxine (T4) and triiodothyronine (T3) profiles and deiodinase enzyme activities in liver, kidney and skin tissues was determined. Types II and III deiodinase enzymes were found to be present in goat skin but not type I. It was concluded that the supply of T3 within the skin was partly independent of circulating hormone profiles. In experiment 2, goats were treated with PTU, triiodothyronine (T3) and bromocriptine (Br) to decrease T3 availability to tissues and circulating PRL concentrations, respectively. Treatment with Br delayed the spring rise in plasma PRL concentrations (P=0.06) and primary (P<0.05) hair follicle activity, and delayed moult onset (P<0.01). PTU treatment did not significantly affect hair follicle activity but generally delayed the time of moult onset (P<0.05). The effects of the treatments were not additive, indicating that the actions of the two hormones were not independent. The effects of PTU and Br treatments were not exerted through changes in IGF-I binding activity in the skin, but binding was greater (P<0.01) in April than November. In experiment 3, treatment with bovine somatotropin (bST), T4 or metoclopramide to increase circulating concentrations of GH, T4 or PRL, failed to prolong the period of anagen in hair follicles, but bST increased fibre growth rate (P<0.05) and this was associated with higher circulating IGF-I concentrations. It is concluded that manipulation of the cycle of the cashmere-producing hair follicle is unlikely to be achieved through manipulation of circulating hormone concentrations alone and that much regulation of hair follicle activity occurs within the skin itself, possibly through changes in enzymes that control the supply of T3 to the follicles, in hormone receptor activity, and in the rate of synthesis of IGF-I and other growth factors within the skin.

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30

Xing, Ti. "Hormone binding in plants." Thesis, De Montfort University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.280511.

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31

Ogawa, Shuichiro. "Abundant expression of the membrane-anchored protease-regulator RECK in the anterior pituitary gland and its implication in the growth hormone/insulin-like growth factor 1 axis in mice." Kyoto University, 2020. http://hdl.handle.net/2433/254494.

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32

Davies, Mina C. G. "Factors affecting embryo mortality in ewe lambs." Thesis, Aberystwyth University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.340852.

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33

Kearney, Tara Maria. "The effect of growth hormone replacement (GHR) apolipoprotein B100 (apoB) kinetics in growth hormone deficient (GHD) hypopituitary subjects." Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.272425.

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34

Smith, Jamie C. "The effects of growth hormone on vascular reactivity and oxidative stress in hypopituitary adults with growth hormone dificiency." Thesis, Cardiff University, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.402851.

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35

Wang, Ying. "Molecular and functional characterization of the prolactin receptor, prolactin-releasing peptide receptor, and growth hormone-releasing hormone receptor genes in chicken." Click to view the E-thesis via HKUTO, 2007. http://sunzi.lib.hku.hk/HKUTO/record/B39556864.

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36

Roberts, April M. "Steroid hormone treatments alter growth characteristics in transformed human ovarian cell lines." Virtual Press, 2003. http://liblink.bsu.edu/uhtbin/catkey/1265095.

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37

Pircher, Tony J. "Regulation of STAT5 activity by growth hormone /." Stockholm, 1998. http://diss.kib.ki.se/search/diss.se.cfm?19980925pirc.

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38

Rico, Bautista Elizabeth. "Negative regulation of growth hormone (GH) signaling /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-184-9/.

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39

Balthasar, Nina. "Transgenic studies of growth hormone secretagogues physiology." Thesis, University College London (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248212.

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40

Bergan, Heather. "Nutritional Regulation of Growth Hormone-Stimulated Lipolysis." Diss., North Dakota State University, 2014. http://hdl.handle.net/10365/24670.

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41

Bergan-Roller, Heather Elaine. "Nutritional Regulation of Growth Hormone-Stimulated Lipolysis." Diss., North Dakota State University, 2014. https://hdl.handle.net/10365/27321.

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Growth hormone (GH) regulates several physiologic processes in vertebrates, including the promotion of growth, an anabolic process, and mobilization of stored lipid, a catabolic process. Here, we used rainbow trout (Oncorhynchus mykiss) as a model to examine the nutritional programming required for the disparate metabolic actions of GH, specifically lipolysis. Juvenile trout were exposed to fed and fasting regimens in vivo and subsequent hormone treatment in vitro. We used real-time quantitative-PCR to measure levels of mRNA expression of Hormone-sensitive lipase 1 (HSL1) and HSL2 in liver, muscle, and adipose tissue. We used Western blotting to investigate the signaling pathways affected by nutritional state and activated by GH (e.g., JAK-STAT, MAPK, PI3K-AKT, PKC-PLC). In vivo, fasting retarded growth and activated lipolysis through enhanced HSL mRNA expression and protein activation. Moreover, fasting resulted in phosphorylation of ERK and PKC but not Akt, JAK2, and STAT5 in adipose tissue, liver, and muscle. In vitro, GH stimulated glycerol release, HSL mRNA expression, and HSL phosphorylation in a time- and concentration- related manner but only in hepatocytes isolated from fasted and not fed fish. Moreover, these actions were dependent upon PKC-PLC and MAPK-ERK activation but not JAK-STAT or PI3K-Akt action. Nutritional state, insulin, and insulin-like growth factor I (IGF-I) pretreatments affect lipolytic responsiveness in hepatocyte. When in a fed state, with high levels of insulin and IGF, GH links to JAK-STAT pathways to promote growth. In a fasted state, with low levels of insulin and IGF, GH links to lipolysis through PKC and ERK activation. The findings of this dissertation indicate that nutritional status of an organism may mediate the pleiotropic actions of GH by linking it to unique intracellular signaling pathways. In the circumstances of fasting, GH stimulates lipolysis through PKC and ERK activation.
National Science Foundation (NSF)
ND EPSCoR
North Dakota State University. Deptartment of Biological Sciences

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42

Pultz, Joseph Anthony. "A stochastic model for growth hormone concentration /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942476405415.

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43

Brittain, Alison Louise. "Growth Hormone (GH) and the Glomerular Podocyte." Ohio University / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1554208861914841.

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44

Dunham, Lee. "Dynamic regulation of growth hormone gene transcription." Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/dynamic-regulation-of-growth-hormone-gene-transcription(62354b9b-c755-43b6-a3f0-d108c32232c9).html.

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Many genes demonstrate highly dynamic pulsatile expression, with characteristic bursts of activity. Dynamic expression of the human prolactin (hPrl) gene in pituitary cells has previously been investigated identifying key temporal characteristics, influenced by the process of chromatin remodelling. Earlier work on the related pituitary human growth hormone (hGH) proximal promoter (-496/+1bp) indicated that it displayed similar dynamic behaviour. The human GH gene contains an extensive long-distance regulatory sequence, including a locus control region (-14/-32kbp) that has been shown to regulate chromatin remodelling and confer tissue-specificity of hGH expression. In this work I aimed to study dynamic regulation of the hGH gene promoter in detail. Initially I investigated the efficiency of several methods to express the luciferase gene in a 180kb hGH genomic fragment using bacterial artificial chromosome recombineering, to allow the investigation of single cell transcription dynamics. Although a functional recombinant BAC was not finalised during the course of the work, I carried out detailed time course studies using shorter hGH-reporter constructs. Using quantitative microscopy to study live single cells, I compared the dynamic characteristics of a 5kb hPrl promoter fragment with those of -840/+1bp and -3348/+1bp hGH-luciferase promoter-reporter constructs. Whilst previous hPrl analysis utilised a binary mathematical model assuming a simplified two-state (ON/OFF) process of gene transcription, I validated and applied a novel stochastic switch model (SSM), assuming instead that transcription rate can switch between any variable states at any time. Through doing so I observed an asymmetry in transcription rate switching, suggesting an all-or-nothing activation of a single UP-switch, with a greater number of rate decreasing DOWN-switches. The -3348/+1bp construct produced double the number of DOWN-switches, whilst the -840/+1bp construct produced 1.5 DOWN-switches in a 48h period. The cycling of transcriptional activity seen by the shorter construct was modified through the addition of forskolin, activating cAMP signalling. However, significant modification of the transcriptionally inactive refractory period seen with the -3348/+1bp construct (reduced from 3h to 1.9h) required histone modification through application of trichostatin A, a HDAC inhibitor. In conclusion, different promoter elements confer different transcriptional timing and dynamics. A subtler transcriptional modelling, such as used here in the SSM, reveals new insights into the phenomena of transcriptional switching, but the mechanisms involved remain to be determined.

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45

Digirolamo, Douglas J. "Growth hormone signaling and action in osteoblasts." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2008. https://www.mhsl.uab.edu/dt/2009r/digirolamo.pdf.

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46

Kabeer, Muhammad Asif. "The immunohistochemical evaluation of thyroid hormone and growth hormone receptors in colorectal carcinoma." Thesis, University of Exeter, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.530383.

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Chan, Koon-wing. "Molecular cloning and functional characterization of a goldfish growth hormone-releasing hormone receptor /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B18539683.

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48

Beswick, Naomi Simone. "The influence of recombinant bovine growth hormone and growth hormone releasing factor on fat synthesis in primiparous Holstein cows." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq22570.pdf.

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49

List, Edward Owen. "Creating Growth Hormone Resistance in Cells using a Hammerhead Ribozyme Approach." Ohio University / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou997813564.

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Bracken, Cynthia J. "Factors controlling ovarian follicular growth in sows /." free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3115527.

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Dissertations / Theses on the topic 'Growth hormone'

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