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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Growth hormone secretion was assessed in nine control subjects and nine patients with Huntington's chorea. 2. Early-morning fasting plasma samples from patients with Huntington's chorea contained abnormally high concentrations of growth hormone. 3. The suppression of growth hormone after oral glucose in choreic patients, unlike the control subjects, occurred at irregular intervals after the glucose was given and was followed, again at irregular intervals, by an exaggerated rebound phase. 4. The response to intravenous insulin was not markedly abnormal in choreic patients. However, there was a significant increase in the rate of rise of growth hormone concentration in the first half and hour after the insulin injection when compared with control subjects.
Clin Sci Mol Med 1976 Jun
PMID:Plasma growth hormone concentrations in Huntington's chorea. 13 32

Mouse kidney beta-glucuronidase production is under multihormonal control. In normal mice, kidney glucuronidase is induced over 100-fold by testosterone. However, hypophysectomy reduces this induction to about 5% of normal. This loss in inducibility was in part restored by growth hormone. Simultaneous administration to hypophysectomized female mice of growth hormone and testosterone, but not of prolactin and testosterone, restored kidney glucuronidase concentration to half that found in testosterone-treated normal female mice. Growth hormone alone had no effect in hypophysectomized females nor did it enhance glucuronidase activity in testosterone-treated normal females. Radiolabeling experiments demonstrated that the enhancement by growth hormone of glucuronidase activity was accompanied by a corresponding increase in its rate of synthesis. Kidney hypertrophy and kidney glucuronidase production may be under common hormonal regulation. Testosterone or growth hormone treatment alone of hypophysectomized mice had little or no effect on either process, but combined treatment with the two hormones significantly enhanced both. The rate of synthesis of kidney glucuronidase is controlled by the Gur gene. Relative differences in kidney glucuronidase synthesis in mice of different Gur genotype were maintained in testosterone-treated hypophysectomized mice. This suggests that control of glucuronidase synthesis by the Gur locus is exerted by interaction with androgens rather than pituitary products.
Mol Cell Endocrinol 1978 Nov
PMID:Roles of growth hormone and testosterone in the synthesis of mouse kidney glucuronidase. 72 3

A somatomedin A preparation, when given at total doses of 14 and 70 U did not increase the longitudinal bone growth in hypophysectomized rats. Growth hormone (WHO) significantly increased the longitudinal bone growth.
Mol Cell Endocrinol 1977 Jan
PMID:Human somatomedin A and longitudinal bone growth in the hypophysectomized rat. 83 64

The medaka (Oryzias latipes) is an egg-laying fresh-water fish. We describe the medaka as a model system of transgenic fish in germs of biological characteristics, manipulation of embryos, gene expression in development, and basic research in aquaculture. The fish are small (approximately 3 cm in length) and have a short generation time (approximately 3 months). The eggs are easy to manipulate. A foreign gene (e.g., the chicken delta crystallin gene) is transferred and expressed stage-dependently in development of medaka embryos. Growth hormone genes of vertebrates are transferred and expressed and, in some cases, accelerate growth of the fish. Thus, the medaka is one of the most promising models of transgenic fish for basic research of gene expression and aquaculture.
Mol Mar Biol Biotechnol
PMID:Medaka as a model of transgenic fish. 130 24

Lactotroph hyperplasia is a prominent finding in the adenohypophyses of pregnant women. In order to elucidate the morphogenesis of this change, pituitaries from 16 women in various phases of pregnancy were collected at autopsy and studied by histology, immunocytochemistry and in situ hybridization. The results showed that the increase in the amount of prolactin (PRL) mRNA paralleled the progressive lactotroph hyperplasia. The presence of mitoses in PRL-immunoreactive cells provided evidence that proliferation of preexisting lactotrophs contribute to lactotroph accumulation. Growth hormone (GH) immunoreactive cells showed a marked reduction in GH mRNA indicating that GH synthesis was inhibited. In many GH-immunoreactive cells, PRL mRNA became apparent. These findings demonstrate that GH is stored following discontinuation of GH synthesis. It appears that, when PRL is secreted in excess during pregnancy, somatotrophs are recruited to produce PRL. These somatotrophs begin to express PRL mRNA, transform to bihormonal mammosomatotrophs and possibly later to lactotrophs, contributing to PRL production. Mature somatotrophs may be regarded as reserve cells in the adenohypophysis, having the potential to switch hormone synthesis and to convert to mammosomatotrophs and possibly lactotrophs.
Virchows Arch B Cell Pathol Incl Mol Pathol 1992
PMID:Pituitary lactotrophs and somatotrophs in pregnancy: a correlative in situ hybridization and immunocytochemical study. 135 2

Growth hormone has been established as a primary regulator of IGF-I gene expression in adults, not only in liver but also in many extrahepatic tissues. We considered the possibility that IGF-I production by adult rat liver could also be stimulated by epidermal growth factor (EGF), a peptide known to be involved in liver regeneration. Chromatographic analysis performed after acid treatment of conditioned media revealed the presence of both immunoreactive (IR) IGF-I and IGF binding protein (IGFBP). Both IR IGF-I and IGFBP were present in the conditioned medium of adult rat hepatocytes in basal conditions. The stimulation of IGF-I and IGFBP secretion by EGF appears to be dose-dependent with a significant increment already evident at 5 nM. That EGF stimulates secretion is supported by the finding that IGF-I and IGFBP-1 mRNA levels are increased after EGF supplementation. We conclude that adult rat hepatocytes spontaneously produce IGF-I and IGFBP, and that EGF is able to increase their synthesis and secretion. This non-growth hormone-dependent regulation of IGF-I and IGFBP-1 production by adult rat hepatocytes in culture indicates an important autocrine/paracrine role for IGF-I, particularly during liver regeneration after extensive organ mass loss.
Mol Cell Endocrinol 1992 Mar
PMID:Effect of epidermal growth factor on insulin-like growth factor-I (IGF-I) and IGF-binding protein synthesis by adult rat hepatocytes. 137 98

Growth hormone (GH) is an important regulator of postnatal growth, acting on a wide variety of target tissues. Here, we show that local production of GH in osteoblasts is able to stimulate bone growth directly without significant systemic effects. Mice were made transgenic by microinjection of an osteocalcin-human GH (osteocalcin-hGH) gene construct in which approximately 1,800 bp of the rat osteocalcin promoter was fused to the hGH gene. Five lines of transgenic mice, each with measurable amounts of serum hGH (ranging from 1 to 1,000 ng/ml), were analyzed. Northern (RNA) blot hybridization showed that the hGH transcript was detectable only in the bone. Further characterization of hGH mRNA distribution by in situ hybridization revealed that in neonates the most intense signal was found in periosteal osteoblasts, while in adults, trabecular and endosteal osteoblasts were favored. In one transgenic line (992-1), hGH was expressed at a much lower level and had minimal systemic effects; however, the local concentrations of hGH in bone were sufficient to stimulate bone growth in these animals.
Mol Cell Biol 1992 Dec
PMID:Osteoblast-specific expression of growth hormone stimulates bone growth in transgenic mice. 144 85

To investigate the effects of sex hormones on 5 alpha-reductase, we examined 5 alpha-reductase mRNA content and enzyme activity in the adrenal cortex of peripubertal male and female rats. In male rats, the influence of castration or hormone-replacement treatment with dihydrotestosterone (5 alpha-DHT) on 5 alpha-reductase was assessed. To stimulate ovarian sex hormone production in immature female rats, the effect of a single injection of 5 IU pregnant mare serum gonadotrophin (PMSG) on 5 alpha-reductase was examined. The efficacy of the treatments was demonstrated by measuring serum LH and ventral prostate weight in male rats, and serum oestradiol and ovarian weight in female rats. Growth hormone was also measured across all treatments in male and female rats. Adrenal 5 alpha-reductase mRNA levels were determined by RNA blot analysis utilizing a rat 5 alpha-reductase cDNA as probe. 5 alpha-Reductase enzyme activity was estimated by isolating [3H]5 alpha-DHT by thin-layer chromatography after incubation with [3H]testosterone. The identity of the [3H]5 alpha-DHT formed was demonstrated by recrystallization of the derivatized DHT to constant specific activity. In controls, adrenal cortical 5 alpha-reductase mRNA content was nearly four times higher in immature female rats compared with intact peripubertal males. Castration resulted in a sevenfold increase in adrenal 5 alpha-reductase mRNA content compared with that in intact controls, while in DHT-injected castrated animals the mRNA level was nearly undetectable. The content of adrenal 5 alpha-reductase mRNA in anoestrous rats was nearly four times higher than in PMSG-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)
J Mol Endocrinol 1991 Apr
PMID:Rat adrenal 5 alpha-reductase mRNA content and enzyme activity are sex hormone dependent. 204 43

Growth hormone (GH) is known to be involved in the control of rat hepatic drug and steroid metabolism through its action on cytochrome P-450s. To examine the role of GH in the regulation of cytochrome P-450f (P-450f), a full-length cDNA clone corresponding to P-450f was isolated and the 3'-non-coding region was utilized for Northern and slot-blot analyses. P-450f mRNA levels were low in neonates, increased after age 4 weeks in male and female rats, and were approximately 3 times higher in the liver of adult female rats than male rats. Hypophysectomy caused a significant decrease in P-450f mRNA levels in male and female rats. Intermittent injection with human growth hormone (hGH) to mimic the male secretory pattern of GH caused a 9-fold increase in P-450f mRNA in hypophysectomized male rats to levels near male control levels, whereas continuous administration of hGH to mimic the female secretory pattern caused a greater increase in P-450f mRNA levels in male and female hypophysectomized rats (25-fold and 9-fold respectively) to levels nearer female control levels. The responses of the other GH-stimulated P-450s, P-450-male and P-450-female, to the different modes of hGH treatment were different from that of P-450f. Since sex hormones are known to affect the regulation of other P-450s, the effect of sex hormones on P-450f mRNA was studied. Ovariectomy caused a 2.4-fold reduction in P-450f mRNA which was partially reversed by estradiol treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
Mol Cell Endocrinol 1990 Jan 02
PMID:Effect of growth hormone on rat hepatic cytochrome P-450f mRNA: a new mode of regulation. 230 59

The mechanism by which tripeptide aldehyde proteinase inhibitors decrease prolactin (PRL) and growth hormone (GH) secretion was studied. Agents known to modify the intracellular levels of cyclic adenosine monophosphate (cAMP) or cytosolic free calcium were used in monolayer cultures of the rat anterior pituitary gland. The phosphodiesterase inhibitor isobutyl-methylxanthine (IBMX), 8-bromo-cAMP and forskolin all stimulated PRL release. Boc-D-Phe-Pro-arginal (Boc-DPPA) at 1 mmol/l concentration was a potent inhibitor of basal PRL release and significantly decreased the effect of 8-Br-cAMP, forskolin or IBMX (0.5 mmol/l). Forskolin (1 mumol/l) stimulated ACTH, PRL and GH release and all these effects were decreased by 100 mumol/l of Boc-D-Phe-Phe-lysinal (Boc-DPPL). Neither tripeptide aldehyde affected the forskolin-induced rise in intracellular cAMP. Growth hormone releasing factor (hpGRF, 1 nmol/l) stimulated both GH release and intracellular cAMP generation; Boc-DPPL (100 mumol/l) significantly decreased stimulated GH release without affecting cAMP accumulation. Increasing medium K+ to 10 times normal level stimulated PRL release presumably by enhancing Ca2+ entry into the cells and 1 mmol/l Boc-DPPA decreased high potassium-stimulated PRL release. The ionophore A-23187 stimulated PRL release at 10 mumol/l but not at 1 mumol/l. At 1 mumol/l A-23187 prevented the Boc-DPPA-induced inhibition of PRL release. These findings suggest that the tripeptide aldehyde proteinase inhibitors inhibit PRL and GH release at a site beyond cAMP formation.
Mol Cell Endocrinol 1987 Jul
PMID:Is calcium or cyclic AMP involved in the inhibitory effect on pituitary hormone secretion of the tripeptide aldehyde proteinase inhibitors? 244 48


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