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Journal articles on the topic 'Growth hormone'

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Author: Grafiati

Published: 4 June 2021

Last updated: 29 July 2024

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1

Diamanti-Kandarakis, Evanthia, Dimitrios Tsilakis, Stefanos Lazarides, Helen Kandarakis, and Angeliki Bergele. "Hormones in sports: growth hormone abuse." HORMONES 3, no. 1 (January 15, 2004): 37–45. http://dx.doi.org/10.14310/horm.2002.11108.

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2

Makras, Polyzois, Dimitris Papadogias, Grigoris Kaltsas, Nikolaos Kaklas, and Georgios Piaditis. "Growth without growth hormone (GH): A case report." HORMONES 3, no. 4 (October 15, 2004): 259–65. http://dx.doi.org/10.14310/horm.2002.11135.

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3

Smith, P. J., and C. G. Brook. "Growth hormone releasing hormone or growth hormone treatment in growth hormone insufficiency?" Archives of Disease in Childhood 63, no. 6 (June 1, 1988): 629–34. http://dx.doi.org/10.1136/adc.63.6.629.

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4

Lippman, Marc E., and Robert B. Dickson. "Growth control of normal and malignant breast epithelium." Proceedings of the Royal Society of Edinburgh. Section B. Biological Sciences 95 (1989): 89–106. http://dx.doi.org/10.1017/s0269727000010587.

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SynopsisWe review information highlighting the multiple roles of both steroidal (primarily oestrogen) and polypeptide regulators of mammary epithelial cell growth, emphasising the work of our laboratory. Effects of both classes of hormones are complex and involve multiple interactions with non-tumour, host tissue. Oestrogen may induce growth regulatory polypeptide growth factors and interact with them in hormone dependent breast cancer. Progression of hormone-dependent breast cancer to hormone independence may involve multiple genetic mechanisms of oncogene activation, loss of the oestrogen receptor, or loss of hormone responsivity of other gene products. Initial carcinogenesis and progression of mammary epithelium to cancer probably also requires both proliferative stimuli (oestrogen, polypeptide growth factors) and genetic damage, leading to qualitatively different hormonal responses (hormone responsive cancer). Future therapies should be designed to block hormonal stimulation better and to interfere with necessary activated or induced components of malignant progression such as oncogenes or polypeptide growth factors receptor systems.

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5

Vance, M. L. "Growth-hormone-releasing hormone." Clinical Chemistry 36, no. 3 (March 1, 1990): 415–20. http://dx.doi.org/10.1093/clinchem/36.3.415.

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Abstract Growth-hormone-releasing hormone (GHRH, somatoliberin) is the hypothalamic peptide hormone that specifically stimulates synthesis and release of growth hormone (GH, somatotropin) by somatotrope cells of the anterior pituitary gland. GHRH is the last of the classically postulated hypothalamic hormones to be characterized, synthesized, and used in clinical medicine. In this review of GHRH, I discuss the discovery and characterization of the peptide, its role in the regulation of GH secretion, and its clinical use in pathological states of GH excess and GH deficiency. The two most clinically useful aspects of GHRH are to establish the etiology of GH deficiency, most commonly the result of a hypothalamic GHRH deficiency, and to treat GH-deficient children. Use of GHRH as therapy for GH deficiency currently is experimental and, to date, results encourage the idea of a therapeutic role for this peptide in promoting endogenous GH secretion with resulting acceleration of linear growth.

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6

Belgorosky, A., A. Martinez, J. J. Heinrich, and M. A. Rivarola. "Lack of correlation of serum estradiol with growth velocity during male pubertal growth." Acta Endocrinologica 120, no. 5 (May 1989): 579–83. http://dx.doi.org/10.1530/acta.0.1200579.

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Abstract. The adolescent growth spurt in boys is under hormonal control. It is accepted that androgens and growth hormone contribute to male pubertal growth, but the role of estrogens is uncertain even though low-dose estradiol administration stimulates growth in prepubertal boys. In the present work, the correlation of serum testosterone and serum estradiol with growth velocity was studied in 16 pubertal normal boys. The study included correlations of growth velocity with serum nonsex hormone-binding globulin-bound testosterone and with serum nonsex hormone-binding globulin-bound estradiol, which are parameters of serum bioavailable sex hormones. A statistically significant positive correlation was found between serum testosterone and growth velocity but not between serum estradiol and growth velocity. These findings are against the hypothesis that estrogens play a growth promoting role during male puberty.

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7

Clapp, Carmen, Stéphanie Thebault, Michael C. Jeziorski, and Gonzalo Martínez De La Escalera. "Peptide Hormone Regulation of Angiogenesis." Physiological Reviews 89, no. 4 (October 2009): 1177–215. http://dx.doi.org/10.1152/physrev.00024.2009.

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It is now apparent that regulation of blood vessel growth contributes to the classical actions of hormones on development, growth, and reproduction. Endothelial cells are ideally positioned to respond to hormones, which act in concert with locally produced chemical mediators to regulate their growth, motility, function, and survival. Hormones affect angiogenesis either directly through actions on endothelial cells or indirectly by regulating proangiogenic factors like vascular endothelial growth factor. Importantly, the local microenvironment of endothelial cells can determine the outcome of hormone action on angiogenesis. Members of the growth hormone/prolactin/placental lactogen, the renin-angiotensin, and the kallikrein-kinin systems that exert stimulatory effects on angiogenesis can acquire antiangiogenic properties after undergoing proteolytic cleavage. In view of the opposing effects of hormonal fragments and precursor molecules, the regulation of the proteases responsible for specific protein cleavage represents an efficient mechanism for balancing angiogenesis. This review presents an overview of the actions on angiogenesis of the above-mentioned peptide hormonal families and addresses how specific proteolysis alters the final outcome of these actions in the context of health and disease.

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8

Avsar, O., S. Sancak, I. Koroglu, and E. Avcı. "Growth hormone, growth hormone receptor and insulin-like growth factor serum levels in patients with obesity and food addiction." Ukrainian Biochemical Journal 93, no. 6 (December 20, 2021): 70–75. http://dx.doi.org/10.15407/ubj93.06.070.

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9

Richalet, Jean-Paul, Murielle Letournel, and Jean-Claude Souberbielle. "Effects of high-altitude hypoxia on the hormonal response to hypothalamic factors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 6 (December 2010): R1685—R1692. http://dx.doi.org/10.1152/ajpregu.00484.2010.

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Acute and chronic exposure to high altitude induces various physiological changes, including activation or inhibition of various hormonal systems. In response to activation processes, a desensitization of several pathways has been described, especially in the adrenergic system. In the present study, we aimed to assess whether the hypophyseal hormones are also subjected to a hypoxia-induced decrease in their response to hypothalamic factors. Basal levels of hormones and the responses of TSH, thyroid hormones, prolactin, sex hormones, and growth hormone to the injection of TRH, gonadotropin-releasing hormone, and growth hormone-releasing hormone (GHRH) were studied in eight men in normoxia and on prolonged exposure (3–4 days) to an altitude of 4,350 m. Thyroid hormones were elevated at altitude (+16 to +21%), while TSH levels were unchanged, and follicle-stimulating hormone and prolactin decreased, while leutinizing hormone was unchanged. Norepinephrine and cortisol levels were elevated, while no change was observed in levels of epinephrine, dopamine, growth hormone (GH), IGF-1, and IGFBP-3. The mean response to hypothalamic factors was similar in both altitudes for all studied hormones, although total T4 was lower in hypoxia during 45 to 60 min after injection. The effect of hypoxia on the hypophyseal response to hypothalamic factors was similar among subjects, except for the GH response to GHRH administration. We conclude that prolonged exposure to high-altitude hypoxia induces contrasted changes in hormonal levels, but the hypophyseal response to hypothalamic factors does not appear to be blunted.

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10

Krukowska-Andrzejczyk, Barbara, Maria Kalina, and Barbara Kalina-Faska. "Effects of Treatment with Recombinant Growth Hormone in Children with Transient Partial Growth Hormone Deficiency – preliminary report." Pediatric Endocrinology 12, no. 1 (2013): 29–36. http://dx.doi.org/10.18544/ep-01.12.01.1438.

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11

Saenger, P. "Growth hormone in growth hormone deficiency." BMJ 325, no. 7355 (July 13, 2002): 58–59. http://dx.doi.org/10.1136/bmj.325.7355.58.

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12

Carel, J. C. "Growth hormone in growth hormone deficiency." BMJ 325, no. 7371 (November 2, 2002): 1037c—1037. http://dx.doi.org/10.1136/bmj.325.7371.1037/c.

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13

Savage, Martin, Helen Storr, Ashley Grossman, and Gerasimos Krassas. "Growth and growth hormone secretion in paediatric Cushing's disease." HORMONES 2, no. 2 (April 15, 2003): 93–97. http://dx.doi.org/10.14310/horm.2002.1187.

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14

Rogol, Alan D., Robert M. Blizzard, Thomas P. Foley, Richard Furlanetto, Richard Selden, Kelly Mayo, and Michael O. Thorner. "Growth Hormone Releasing Hormone and Growth Hormone: Genetic Studies in Familial Growth Hormone Deficiency." Pediatric Research 19, no. 5 (May 1985): 489–92. http://dx.doi.org/10.1203/00006450-198505000-00016.

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15

Mericq, V., F. Cassorla, H. Garcia, A. Avila, Cy Bowers, and G. Merriam. "1 GROWTH HORMONE RESPONSES TO GROWTH HORMONE RELASING REPTIDE (GRP) AND TO GROWTH HORMONE RELEASING HORMONE (GRF) IN GROWH HORMONE DIFFICIENT CHILDREN (GND)." Pediatric Research 36, no. 5 (November 1994): 672. http://dx.doi.org/10.1203/00006450-199411000-00025.

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16

Valcavi, R., M. Zini, and I. Portioli. "Thyroid hormones and growth hormone secretion." Journal of Endocrinological Investigation 15, no. 4 (April 1992): 313–30. http://dx.doi.org/10.1007/bf03348744.

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17

Markova, T. N., E. V. Kosova, and N. K. Mishchenko. "Pituitary disorders in patients with end-stage chronic renal failure." Problems of Endocrinology 69, no. 6 (January 24, 2024): 37–46. http://dx.doi.org/10.14341/probl13212.

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Disorders in the kidneys lead to disturbance of homeostasis. As the glomerular filtration rate decreases, the metabolism of numerous biologically active substances, including pituitary hormones, decreases. The article presents an overview of pituitary dysfunction in patients with chronic kidney disease (CKD) and discusses the possible reasons of the pathogenetic mechanisms. Particular focus is being given to the assessment of changes in the concentration of pituitary hormones in patients with end-stage chronic kidney disease (CKD) and discusses the pathogenetic mechanisms of their formation. Particular attention is paid to the assessment of changes in the concentration of pituitary hormones in patients receiving renal replacement therapy (RRT). CKD leads to an increase in the level of prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Concentrations of growth hormone (GH), isulin-like growth factor-1 (IGF-1), thyroid-stimulating hormone (TSH), adrenocorticotropic hormone (ACTH) and vasopressin may remain within normal values or increase in this group of patients. RRT does not reduce the levels of prolactin, LH, FSH, while the concentration of growth hormone, IGF-1, TSH tends to normalize. The content of ACTH and vasopressin may remain unchanged or decrease. Kidney transplantation in most cases corrects hormonal disorders. Correction of hormonal changes can improve the clinical outcome and quality of life of patients with end stage CKD.

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18

Butenandt, O., and B. Staudt. "Comparison of growth hormone releasing hormone therapy and growth hormone therapy in growth hormone deficiency." European Journal of Pediatrics 148, no. 5 (February 1989): 393–95. http://dx.doi.org/10.1007/bf00595894.

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19

Amal, Rizki Jaya, Irfansyah, Muhammad Arif Hasan, and Aulia Putra Rahman. "Analysis of Studies on the Role of Hormones in Micropenis Disorders: A Systematic Literature Review." Open Access Indonesian Journal of Medical Reviews 3, no. 6 (November 21, 2023): 528–33. http://dx.doi.org/10.37275/oaijmr.v3i6.420.

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A deep understanding of the role of specific hormones in genital development is key to designing effective therapeutic approaches. Factors such as testosterone deficiency, growth hormone disorders, or other hormonal imbalances can be targets for hormonal interventions that can affect penis size. This study aimed to explore the role of hormonal aspects in micropenis disorders. The literature search process was carried out on various databases (PubMed, Web of Sciences, EMBASE, Cochrane Libraries, and Google Scholar) regarding the role of hormonal aspects in micropenis disorders. This study follows the preferred reporting items for systematic reviews and meta-analysis (PRISMA) recommendations. Aspects of the hormonal role in micropenis include several key elements that influence the development of genital organs in men. Hormones, such as testosterone, growth hormone, estrogen, and dihydrotestosterone (DHT), play an important role in stimulating penis growth and development. Proper hormonal balance is necessary for normal genital development, and disturbances in the production of or response to these hormones may contribute to conditions such as micropenis.

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20

Gelato, Marie C. "Growth Hormone-Releasing Hormone." Endocrinologist 4, no. 1 (January 1994): 64–68. http://dx.doi.org/10.1097/00019616-199401000-00010.

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21

Savage, M. O., and G. M. Besser. "Growth hormone releasing hormone." Archives of Disease in Childhood 60, no. 5 (May 1, 1985): 405–6. http://dx.doi.org/10.1136/adc.60.5.405.

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22

FROHMAN, LAWRENCE A., and JOHN-OLOV JANSSON. "Growth Hormone-Releasing Hormone*." Endocrine Reviews 7, no. 3 (August 1986): 223–53. http://dx.doi.org/10.1210/edrv-7-3-223.

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23

Gelato, Marie C. "Growth Hormone-Releasing Hormone." Endocrinologist 15, no. 3 (May 2005): 159–64. http://dx.doi.org/10.1097/01.ten.0000162232.25674.d6.

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24

Gelato, M. C., and G. R. Merriam. "Growth Hormone Releasing Hormone." Annual Review of Physiology 48, no. 1 (October 1986): 569–91. http://dx.doi.org/10.1146/annurev.ph.48.030186.003033.

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25

Argente, Jesus, Angelo Acquafredda, Luciano Cavallo, Marcel Donnadieu, and Danièle Evain-Brion. "Growth Hormone-Releasing Hormone." Neonatology 52, no. 5 (1987): 264–67. http://dx.doi.org/10.1159/000242718.

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26

Ross, R. J. M., S. Tsagarakis, A. Grossman, M. A. Preece, C. Rodda, P. S. W. Davies, L. H. Rees, M. O. Savage, and G. M. Besser. "TREATMENT OF GROWTH-HORMONE DEFICIENCY WITH GROWTH-HORMONE-RELEASING HORMONE." Lancet 329, no. 8523 (January 1987): 5–8. http://dx.doi.org/10.1016/s0140-6736(87)90699-4.

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27

de Gennaro Colonna, V., E. Cattaneo, D. Cocchi, E. E. Müller, and A. Maggi. "Growth hormone regulation of growth hormone-releasing hormone gene expression." Peptides 9, no. 5 (September 1988): 985–88. http://dx.doi.org/10.1016/0196-9781(88)90077-0.

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28

Arvat, Emanuela, Laura Gianotti, Roberta Giordano, Fabio Broglio, Mauro Maccario, Fabio Lanfranco, Giampiero Muccioli, et al. "Growth Hormone–Releasing Hormone and Growth Hormone Secretagogue-Receptor Ligands." Endocrine 14, no. 1 (2001): 035–43. http://dx.doi.org/10.1385/endo:14:1:035.

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29

Carlson, H. E., M. L. Graber, M. C. Gelato, and J. M. Hershman. "Endocrine Effects of Erythropoietin." International Journal of Artificial Organs 18, no. 6 (June 1995): 309–14. http://dx.doi.org/10.1177/039139889501800603.

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Uremic men may manifest a variety of hormonal abnormalities, including decreased serum concentrations of testosterone and thyroid hormones and increased serum levels of growth hormone and prolactin. Some previous investigations have reported that erythropoietin therapy may reverse these hormonal changes. To investigate this possibility further, we measured serum prolactin, testosterone, LH, FSH, TSH, free thyroxine, triiodothyronine, growth hormone and IGF-I in 21 generally elderly male hemodialysis patients before and during erythropoietin therapy; many of the patients also received an anabolic steroid or metoclopramide treatment. Despite a significant erythropoietic response in a majority of the subjects, no significant changes were seen in any of the hormonal parameters other than a small decrease in serum growth hormone concentrations. Advanced age and chronic illness in our patients may have played a role in limiting the hormonal response reported by others.

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30

Kovács, P., Y. Nozawa, and G. Csaba. "Induction of hormone receptor formation in the unicellular tetrahymena." Bioscience Reports 9, no. 1 (February 1, 1989): 87–92. http://dx.doi.org/10.1007/bf01117514.

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Studies based on treatment with antibodies to thyrotropic hormone, luteotropic hormone, growth hormone or adrenocorticotropic hormone have shown that although the unicellular Tetrahymena does not possess sui generis receptors to all polypeptide hormones, such binding structures may arise, or become established in the membrane of the unicellular Tetrahymena in the presence of exogenous hormone. The Tetrahymena subjected to hormonal imprinting still contained an increased amount of hormone after six generation changes, which suggested that either hormone production had been induced by treatment, or the internalized hormone had not been degraded intracellularly. Thus the role of hormonal imprinting in receptor formation has also been substantiated by the immunocytochemical approach used in the present study.

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31

Mericq, V., F. Cassorla, H. García, A. Avila, C. Bowers, and G. Merriam. "GROWTH HORMONE RESPONSES TO GROWTH HORMONE RELEASING PEPTIDE (GRP) AND TO GROWTH HORMONE RELEASING HORMONE (GRF) IN GROWTH HORMONE DEFICIENT CHILDREN (GHD)." Pediatric Research 33 (May 1993): S47. http://dx.doi.org/10.1203/00006450-199305001-00263.

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32

Tapanainen, P. J. "Circulating immunoreactive growth hormone releasing hormone concentrations and growth hormone response to growth hormone releasing hormone in short children." European Journal of Pediatrics 152, no. 12 (December 1993): 984–89. http://dx.doi.org/10.1007/bf01957221.

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33

ROOT, Allen W., Dorothy SHULMAN, Jennifer ROOT, and Frank DIAMOND. "The interrelationships of thyroid and growth hormones: effect of growth hormone releasing hormone in hypo- and hyperthyroid male rats." Acta Endocrinologica 113, no. 4_Suppl (December 1986): S367—S375. http://dx.doi.org/10.1530/acta.0.112s367.

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ABSTRACT Growth hormone (GH) and the thyroid hormones interact in the hypothalamus, pituitary and peripheral tissues. Thyroid hormone exerts a permissive effect upon the anabolic and metabolic effects of GH, and increases pituitary synthesis of this protein hormone. GH depresses the secretion of thyrotropin and the thyroid hormones and increases the peripheral conversion of thyroxine to triiodothyronine. In the adult male rat experimental hypothyroidism produced by ingestion of propylthiouracil depresses the GH secretory response to GH-releasing hormone in vivo and in vitro, reflecting the lowered pituitary stores of GH in the hypothyroid state. Short term administration of large amounts of thyroxine with induction of the hyperthyroid state does not affect the in vivo GH secretory response to GH-releasing hormone in this animal.

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34

Mandala, Aletha Yuliana, Ni Ketut Suwiti, and I. Wayan Suardana. "The Growth Hormone Level of Bali Cattle’s Post Treatment with Ethinil Esthradiol and Progesteron Hormones in Combination with Mineral." Journal of Veterinary and Animal Sciences 2, no. 1 (January 31, 2019): 1. http://dx.doi.org/10.24843/jvas.2019.v02.i01.p01.

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This study aims to find out the growth hormone level of bali cattle’s post giving of ethinyl estradiol and progesterone hormones combined with mineral. The total sample of 64 bali cattle is divided into 4: Group I (Control) is not given hormone ethinyl estradiol, progesterone and mineral. Group II is given the hormone ethinyl estradiol and progesterone, without mineral. Group III was not given ethinyl estradiol and progesterone hormones, with mineral administration. Group IV is given hormone ethinyl estradiol, progesterone and mineral. At the end of the study, measurements were performed to determine the growth hormone level using ELISA method. The data of the research were analyzed by the analysis of variance. The result showed that male cattle growth hormone (268.281±73.13pg/ml) was higher than females (236.250±13.79pg/ml). The growth hormone level of young cattle was higher (264.94±74.42pg/ml) than adult (239.59±14.05pg/ml). Level of growth hormone of bali cattle with highest minerals(266.97±74.15pg/ml) compared without minerals (237.56±11.05pg/ml). The growth hormone level of bali cattle with higher levels of ethinyl estradiol and progesterone hormone (263.31±74.81pg/ml) compared with no ethinyl estradiol and progesterone hormone (241.22±18.8pg/ml). The results are age and sex effect on growth hormone level with hormone ethinyl estradiol and progesterone combined with mineral. Giving ethinyl estradiol and progesterone hormones combined with significant mineral (P<0.05) may increase the growth hormone level of young male bali cattle.

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35

Martin, Dr Finbarr C., and Dr Ian Sturgess. "Growth hormone, aging and frailty." Reviews in Clinical Gerontology 9, no. 3 (August 1999): 207–14. http://dx.doi.org/10.1017/s0959259899009326.

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Growth hormone and related growth factors are essential for normal childhood development, secretion rate then declining from early adulthood. Adults with growth hormone deficiency, e.g. after pituitary ablation, have many clinical features such as reduced muscle and bone mass which are also seen in healthy older people. In both cases, growth hormone treatment at least partly reverses these changes. This has led to the rather elegant notion that growth hormone decline may be responsible for age-related involution and death and raises the prospect of hormonal replacement therapy for aging and frailty.

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36

Quigley, Charmian A. "Growth Hormone Treatment of Non–Growth Hormone-Deficient Growth Disorders." Endocrinology and Metabolism Clinics of North America 36, no. 1 (March 2007): 131–86. http://dx.doi.org/10.1016/j.ecl.2006.11.006.

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37

BUTENANDT, O. "Growth hormone-releasing hormone or growth hormone: which one should be used in growth hormone deficient patients?" Acta Endocrinologica 120, no. 3_Suppl (June 1989): S86—S87. http://dx.doi.org/10.1530/acta.0.120s086.

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38

Sudrajat, Agus Oman, Muhammad Muttaqin, and Alimuddin. "Effectivity of thyroxine and recombinant growth hormone on the growth of Siam-catfish larvae." Jurnal Akuakultur Indonesia 12, no. 1 (January 17, 2014): 31. http://dx.doi.org/10.19027/jai.12.31-39.

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<p class="NoParagraphStyle" align="center"><strong>ABSTRACT</strong></p><p class="NoParagraphStyle" align="center"><strong> </strong></p><p class="NoParagraphStyle">Catfish hatchery requires technology and engineering to maximize the development and growth of fish. In this research the hormone thyroxine (T4), recombinant growth hormone (G) and mix of thyroxine and growth hormones (GT) were administered by immersion to enhance the development and growth of stripped catfish larvae. Research was using completely randomized design, with four treatments and five replications; A, control; B, thyroxine hormone (T4) 0.1 mg/L; C, T4 and G (GT) (0.1 mg/L and 10 mg/L); and D, G 10 mg/L. Immersion was performed for one hour. Results showed that the rate of yolk absorption at 16 hours post immersion was higher (P<0.05) in treatment B (96.98%) compared with treatments A (18.54%), C (20.59%), and D (32.90%). Larval growth of treatments B (24.85 mm) and C (24.00 mm) was higher (P<0.05) compared with treatments A (21.71 mm) and D (23.18 mm). Survival among treatments were similar (P>0.05). The size of liver cell and cytoplasm of treated larvae were larger than the control. Behavior of fish in the treatments B and C showed more active than the treatments A and D. Thus, combination of thyroxine and recombinant growth hormone treatment (C) has an efficient of yolk utilization, and higher in development and growth of stripped catfish larvae.</p><p class="NoParagraphStyle"> </p><p class="NoParagraphStyle">Keywords: thyroxine, growth hormone, yolk absorption, growth, stripped catfish</p><p class="NoParagraphStyle"> </p><p class="NoParagraphStyle"> </p><p class="NoParagraphStyle" align="center"><strong>ABSTRAK</strong></p><p class="NoParagraphStyle" align="center"> </p><p class="NoParagraphStyle">Pembenihan ikan patin membutuhkan teknologi dan rekayasa untuk memaksimumkan perkembangan, dan pertumbuhan ikan. Pada penelitian ini dilakukan pemberian hormon tiroksin (T4), hormon pertumbuhan rekombinan (G) serta hormon gabungan antara hormon tiroksin dan hormon pertumbuhan (GT) melalui perendaman untuk memacu perkembangan dan pertumbuhan larva ikan patin siam. Penelitian menggunakan rancangan acak lengkap, dengan empat perlakuan dan lima kali ulangan; A, kontrol; B, hormon tiroksin (T4) 0,1 mg/L; C, T4 dan G (GT) (0,1 mg/L dan 10 mg/L); dan D, G 10 mg/L. Perendaman dilakukan selama satu jam. Hasil penelitian menunjukkan bahwa laju penyerapan kuning telur pada jam ke-16 setelah perendaman lebih cepat (P<0,05) pada perlakuan B (96,98%) dibandingkan dengan perlakuan A (18,54%), C (20,59%), dan D (32,90%). Pertumbuhan larva yang diberi perlakuan B (24,85 mm) dan C (24,00 mm) lebih tinggi (P<0,05) dibandingkan dengan perlakuan A (21,71 mm) dan D (23,18 mm). Tingkat kelangsungan hidup antarperlakuan tidak berbeda (P>0,05). Ukuran sel dan sitoplasma hati ikan perlakuan relatif lebih besar dibandingkan kontrol. Tingkah laku ikan pada perlakuan B dan C lebih aktif dibandingkan perlakuan A dan D. Dengan demikian kombinasi hormon tiroksin dan hormon pertumbuhan rekombinan secara bersama (C) memiliki efisiensi pemanfaatan kuning telur, perkembangan, dan pertumbuhan lebih tinggi pada larva ikan patin.</p><p class="NoParagraphStyle"> </p><p class="NoParagraphStyle">Kata kunci: tiroksin, hormon pertumbuhan, penyerapan kuning telur, pertumbuhan, ikan patin siam</p><p> </p>

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GELATO, MARIE C., ROGER S. RITTMASTER, ORA H. PESCOVITZ, MANUELA CARUSO NICOLETTI, WILBERT E. NIXON, ROSARIO D’AGATA,, D. LYNN LORIAUX, and GEORGE R. MERRIAM. "Growth Hormone Responses to Continuous Infusions of Growth Hormone-Releasing Hormone*." Journal of Clinical Endocrinology & Metabolism 61, no. 2 (August 1985): 223–28. http://dx.doi.org/10.1210/jcem-61-2-223.

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Alba, Maria, and Roberto Salvatori. "Growth Hormone-Releasing Hormone Receptor Mutations in Familial Growth Hormone Deficiency." Endocrinologist 13, no. 5 (September 2003): 422–27. http://dx.doi.org/10.1097/01.ten.0000089866.37355.d3.

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SMITH, P. J., C. G. D. BROOK, J. RIVIER, W. VALE, and M. O. THORNER. "NOCTURNAL PULSATILE GROWTH HORMONE RELEASING HORMONE TREATMENT IN GROWTH HORMONE DEFICIENCY." Clinical Endocrinology 25, no. 1 (July 1986): 35–44. http://dx.doi.org/10.1111/j.1365-2265.1986.tb03593.x.

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Tannenbaum, Gloria Shaffer, and Cyril Y. Bowers. "Interactions of Growth Hormone Secretagogues and Growth Hormone-Releasing Hormone/Somatostatin." Endocrine 14, no. 1 (2001): 021. http://dx.doi.org/10.1385/endo:14:1:021.

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Merriam, George R., Robert S. Schwartz, and Michael V. Vitiello. "Growth Hormone-Releasing Hormone and Growth Hormone Secretagogues in Normal Aging." Endocrine 22, no. 1 (2003): 41–48. http://dx.doi.org/10.1385/endo:22:1:41.

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López, P. Benito, L. Avila, M. S. Corpas, J. A. Jiménez, L. Cacicedo, and F. Sánchez Franco. "Sex differences in growth hormone response to growth hormone-releasing hormone." Journal of Endocrinological Investigation 14, no. 4 (April 1991): 265–68. http://dx.doi.org/10.1007/bf03346809.

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Matsuno, Akira. "Growth Hormone." Journal of Neurosurgery 106, no. 5 (May 2007): 940. http://dx.doi.org/10.3171/jns.2007.106.5.940.

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&NA;. "Growth hormone." Reactions Weekly &NA;, no. 703 (May 1998): 8. http://dx.doi.org/10.2165/00128415-199807030-00026.

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&NA;. "Growth hormone." Reactions Weekly &NA;, no. 440 (February 1993): 9. http://dx.doi.org/10.2165/00128415-199304400-00039.

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&NA;. "Growth hormone." Reactions Weekly &NA;, no. 419 (September 1992): 8. http://dx.doi.org/10.2165/00128415-199204190-00029.

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Harris, Martin. "Growth hormone." Inpharma Weekly &NA;, no. 899 (August 1993): 7. http://dx.doi.org/10.2165/00128413-199308990-00012.

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&NA;. "Growth hormone." Reactions Weekly &NA;, no. 486 (January 1994): 7. http://dx.doi.org/10.2165/00128415-199404860-00029.

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