Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Growth hormone releasing peptide (GHRP-2) is a synthetic hexapeptide which specifically stimulates secretion of growth hormone (GH) by fetal pituitary somatotrophs through a new membrane receptor, which is different from growth hormone releasing hormone (GHRH) and somatostatin (SMS) receptors. We used cell cultures of human fetal pituitary somatotroph cells to investigate the effect of GHRH, GHRP-2 and somatostatin on GH secretion. The results showed that the mechanism of GHRH/SMS and GHRP-2 was different. This indicated that a different intracellular signal transduction system might also play a crucial role in the regulation of GH secretion.
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PMID:The effect of GHRH, GHRP-2 and somatostatin on GH secretion by fetal pituitary. 1293 17

Rab3B is involved in the exocytosis of synaptic vesicles and secretory granules in the central nervous system and the anterior pituitary cells. The aim of this study was to elucidate both the role of rab3B in GH secretion and the mutual relationship of rab3B and SNARE proteins. Adult male rats were injected intravenously with 10 microg of growth hormone releasing hormone (GHRH) or 10 microg of somatostatin (SRIF). Untreated rats were used as controls, and their pituitary glands were sectioned for histochemical examination. Rab3B is localized on the limiting membrane of the secretory granules and the cytosol. Confocal laser scanning microscopic observation of immunohistochemical double staining of rab3B and GH revealed that immunoreactivity of rab3B increased in GHRH-treated rats and decreased in SRIF-treated rats. Confocal laser scanning microscopic observation of immunohistochemical double staining of SNAP-25, syntaxin, and rab3B revealed the co-localization of rab3B and these SNARE proteins in GHRH-treated rats, and their dissociation in SRIF-treated rats. These results suggest that rab3B plays a principal role in GH secretion in the anterior pituitary cells and that SNAP-25 and syntaxin act as co-workers with rab3B in the functional regulation of GH secretion.
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PMID:Dynamics of subcellular organelles, growth hormone, Rab3B, SNAP-25, and syntaxin in rat pituitary cells caused by growth hormone releasing hormone and somatostatin. 1450 89

Growth hormone secretion is under the control of a pair of hypothalamic factors, growth hormone releasing hormone and somatostatin. The growth hormone secretagogue receptor (GHSR) and its endogenous ligand represent a novel third method regulating the release of growth hormone. Early chicken embryonic development has been proposed to be independent of GH. However, recent evidence shows that peripheral GH secretion has paracrine/autocrine functions during embryonic development. In the current study, we used the reverse-transcriptase polymerase chain reaction to determine the expression pattern of the GHSR during embryonic development and the effects of in ovo recombinant human (rh) IGF-I administration on its expression pattern. Eggs were injected once with 100 ng rhIGF-I in 10 mM acetic acid, and 0.1% BSA per embryo on embryonic day 3. Total RNA was isolated from whole embryos on embryonic day (E) 0-6 (n=6 per day), thoracic/abdominal halves of the embryos on E7- E8 (n= 6 per day) and Pectoralis muscle on E9-E20 (n= 4 per day). We found that GHSR expression was low during E0-E4, followed by an increase on E5 and remained constant through E17. GHSR expression then increased on E18 before reducing on E20. A similar pattern was found in the rhIGF-I treated embryos with the exception of a significant increase in GHSR expression on E8. These data indicate that the GHSR may be active in regulating GH secretion during early embryonic development, and upregulation of the GHSR gene following IGF-I administration may have an important role in the determination of postnatal muscle growth.
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PMID:The effects of in ovo rhIGF-I administration on expression of the growth hormone secretagogue receptor (GHSR) during chicken embryonic development. 1530 60

The regulation of growth hormone 1 (GH1) and insulin-like-growth factor-1 (IGF-1) release is under the influence of three pituitary hormones [growth hormone releasing hormone (GHRH), ghrelin (GHRL) and somatostatin (SST)], which act in an autocrine/paracrine fashion in the breast. By binding to their respective receptors, they control cell proliferation, differentiation and apoptosis in a GH1/IGF-1-dependent manner. We investigated single nucleotide polymorphisms (SNPs) in the GHRH, GHRHR, GHRL, GHSR, SST and SSTR2 gene regions in a Polish and a German cohort of 798 breast cancer cases and 1011 controls. Our study revealed an association of a novel TC repeat polymorphism in the SST promoter with a decreased breast cancer risk in the Polish study population [odds ratio (OR), 0.65; 95% confidence interval (CI), 0.44-0.96]. The closely linked SNP IVS1 A+46G showed the same trend. For both polymorphisms the association was stronger in women above the age of 50 (OR, 0.33; 95% CI, 0.14-0.76 and OR, 0.39; 95% CI, 0.18-0.87, respectively). The protective effect of these polymorphisms was confirmed in a haplotype analysis among women above 50 years of age and carrying the two variant alleles (OR, 0.37; 95% CI, 0.17-0.80). In the independent German population, we observed slightly decreased ORs among women above the age of 50 years. In the SSTR2 gene, carriers of the promoter 21/21 TG repeat genotype were at a decreased breast cancer risk (OR, 0.62; 95% CI, 0.41-0.94) compared to carriers of the other genotypes in the Polish population. Furthermore, we identified a protective effect of the GHRHR C-261T SNP in both populations (joint analysis CT+TT versus CC: OR, 0.80; 95% CI, 0.65-0.99). This effect was carried by a haplotype containing the protective allele. Thus, our study concludes a possible protective influence of distinct polymorphisms in genes involved in GH1 release on breast cancer risk.
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PMID:Polymorphisms in genes involved in GH1 release and their association with breast cancer risk. 1660 30

Growth hormone release and IGF-I synthesis decrease with increasing age. The regulation of the GH/IGF-I system is dependent on the integrity of the hypothalamus, pituitary and liver. During aging there are several changes which contribute to the decline in GH/IGF-I including changes in signal to the somatotrophs from growth hormone releasing hormone, somatostatin and other factors such as body composition, exercise, diet and sleep. All of these factors are discussed in detail within this review. The phenotypic similarities between aging and adult growth hormone deficiency syndrome combined with this decrease in GH/IGF-I with aging have prompted the question whether aging is a GH deficient state. The advent of recombinant growth hormone has led to a number of studies treating elderly patients with GH alone or in combination with sex steroids or exercise. The results of these studies would not back up the use of GH in elderly non-hypopituitary patients as they did not show efficacy, showed high rates of adverse events and there is also some evidence associating GH/IGF-I and risk of neoplasia. If GH therapy is to be used in this cohort of patients further long term efficacy and safety studies are required.
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PMID:Aging and the growth hormone/insulin like growth factor-I axis. 1749 9

Patients with anorexia nervosa (AN) may develop multiple endocrine abnormalities, including amenorrhea, hyperactivity of the hypothalamus-pituitary-adrenal axis, hypothyroidism and particular changes in the activity of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis. Exaggerated GH secretion and reduced IGF-I levels are usually found in AN, as well as in conditions of malnutrition and malabsorption, insulin-dependent diabetes mellitus, liver cirrhosis and catabolic states. In AN, GH hypersecretion at least partially reflects malnutrition-induced peripheral GH resistance, which leads to reduced IGF-I synthesis and release; this implies an impairment of the negative IGF-I feedback action on GH secretion. On the other hand, primary alterations in the neural control of GH secretion cannot be ruled out. The neuroendocrine alterations include enhanced somatotroph responsiveness to growth hormone releasing hormone (GHRH) and impaired GH response to most central nervous system-mediated stimuli. Particular resistance to cholinergic manipulation has also been demonstrated, thus suggesting a somewhat specific alteration in the somatostatin (SS)-mediated cholinergic influence on GH secretion. Moreover, paradoxical GH responses to glucose load, thyrotropin releasing hormone (TRH) and luteinizing hormone releasing hormone (LHRH) have also been reported. The effect of reduced leptin levels on GH hypersecretion in AN is still unclear, but ghrelin (the gastric hormone that is a natural ligand of the GH secretagogue receptor and strongly stimulates somatotroph secretion) is thought to play a major role. Regardless of the supposed central and peripheral alterations, it has to be emphasised that the activity of the GH/IGF-I axis in AN is generally restored by nutritional and stable weight gain. It therefore reflects an impaired nutritional state and cannot be considered a primary hallmark of the disease.
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PMID:GH/IGF-I axis in anorexia nervosa. 1764 63

Growth hormone (GH) response to dexamethasone (DEX) in 10 poorly controlled insulin dependent diabetic patients (IDDM) without clinical evidence of diabetic complications and in 10 healthy controls, was studied. GH responses to DEX were compared with pituitary GH response to growth hormone releasing hormone (GHRH). Fasting GH values were not significantly higher in IDDM in comparison with the controls. The peak GH responses to GHRH and DEX were similar in the controls and IDDM patients (23.8 +/- 6.49 vs 38.87 +/- 7.26, p > 0.05 in GHRH test and 13.71 +/- 3.59 vs 17.33 +/- 5 23, p > 0.05 in DEX test). No significant difference between area under curve during GHRH (1386. +/- 490.69 vs 1966.89 +/- 561.46, p > 0.05) and during DEX test (1085.8 +/- 239 856 vs 501.87 +/- 847.16, p > 0 05) in the controls and IDDM patients, were established There was no significant correlation between basal and peak GH values and AUC during both tests, and HbA1C and duration of diabetes It is concluded that GH response to GHRH was normal and that our patients had preserved the integrity of the hypothalamo-pituitary axis, thanks to the suggested mechanism of dexamethasone action via somatostatin.
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PMID:[Effects of dexamethasone on growth hormone response in insulin dependent diabetes mellitus]. 1797 66

Approximately half of patients with HIV-infection develop abnormal body fat distribution, characterized by increased abdominal, breast, and dorsocervical adiposity and decreased fat in the limbs and face in association with antiretroviral therapy. Changes in fat distribution are associated with dyslipidemia, insulin resistance, and increased cardiovascular risk in patients with HIV lipodystrophy. Growth hormone secretion is reduced and responses to standardized stimulation testing altered, suggesting relative growth hormone deficiency in this population. Growth hormone secretion is characterized by normal pulse frequency, but decreased pulse amplitude, pulse width, and trough GH levels compared to weight matched, non-HIV-infected patients. Abnormalities in GH secretion are strongly associated with body composition and metabolic abnormalities in patients with HIV lipodystrophy, particularly with increased visceral fat and elevated free fatty acids. Increased somatostatin tone and decreased ghrelin concentrations may also contribute to reduced GH levels. Administration of exogenous GH or growth hormone releasing hormone (GHRH) to normalize growth hormone concentrations is effective to reduce visceral fat and improve lipid parameters in HIV-infected patients. Treatment with supraphysiologic GH is limited by side effects and exacerbation of insulin resistance, whereas administration of physiologic doses of GH demonstrates more modest treatment effects but fewer adverse effects. Initial studies of GHRH also show significant reductions in visceral adipose tissue (VAT) with potentially fewer adverse effects. GHRH may be particularly useful to normalize GH dynamics in patients with HIV lipodystrophy by increasing endogenous GH pulse height, GH pulse width, and trough GH levels, while preserving the negative feedback of IGF-I on pituitary GH secretion.
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PMID:GH/GHRH axis in HIV lipodystrophy. 1827 Aug 41

The authors present numerous historical descriptions of persons who might suffered from gigantism or acromegaly. The oldest medical data of patients, initial attempts of causal neurosurgical treatment, history of growth hormone, insulin-like growth factor-1, growth hormone releasing hormone and somatostatin discovery is reported. The highest contemporary living persons are also listed.
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PMID:[Acromegaly--from myths to facts]. 1861

Sleep is an essential ubiquitous biological process, a periodical state of quiescence in which there is minimal processing of sensory information and no interaction with conspecifics or the environment. Despite relevant research on sleep structure and testing of numerous endogenous sleep-affecting chemicals, questions as to the precise mechanisms and functions of sleep remain without satisfactory responses. The purpose of this review is to report on current evidence as regards the effect of several endogenous and exogenous hormones, hormonal agents, and neuropeptides on sleep onset or wake process, when administered in humans in specific doses and via different routes. The actions of several peptides are presented in detail. Some of them (growth hormone releasing hormone, ghrelin, galanin, neuropeptide Y) seem to promote sleep, whereas others (corticotropin, somatostatin) impair its continuity.
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PMID:Hormones, hormonal agents, and neuropeptides involved in the neuroendocrine regulation of sleep in humans. 2004 96


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