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)

This review addresses some relevant aspects of the aging of the neuroendocrine system, particularly the reproductive and the adrenocortical axis. Deterioration of the reproductive function, one of the most striking endocrine alterations occurring in aging, is related to a complex interplay of factors. They comprise alterations occurring at the level of all the three components of the reproductive axis, the gonads, the pituitary and the brain, acting synergistically to disrupt the normal pulsatile release of gonadotropins. Particular relevance is given to the neurotoxic action of estrogens during the constant estrous phase occurring in aged female rodents, at the level of hypothalamic nuclei regulating gonadotropin secretion. This effect, to be found also in women during the anovulatory period of the perimenopause, would worsen the dysregulation of the central mechanisms controlling the reproductive function. The activity of the adrenocortical (HPA) axis increases with advancing age in rodents but also, although less strikingly, in humans. The main alteration which can be evidenced in both species is a delayed post-stimulus decline in plasma corticosteroid levels, indicating a diminished sensitivity to glucocorticoids of HPA axis feedback regulation in the elderly. Increased exposure to the highly catabolic adrenal glucocorticoids appears to be associated to a loss of cerebral neurons, particularly in the hippocampus, and the emergence of cognitive deficits in the aged rats. The relevance of experimental data performed in rodents to healthy and pathological human aging is extensively discussed. Finally, this chapter considers the age-related impairment in growth hormone secretion, a common finding of all the animal species investigated so far. The etiology of the hyposomatotropism of aging is namely linked to a progressive defect in growth hormone releasing hormone-producing hypothalamic neurons, although alterations of somatostatin-producing neurons have also been described. This background knowledge makes the use of neuroactive compounds aimed at restoring the physiologic function of hypothalamic hypophysiotropic hormones a rational approach to rectify the alterations of the neuroendocrine system occurring in elderly individuals.
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PMID:Age-related alterations in gonadotropin, adrenocorticotropin and growth hormone secretion. 132 12

A variety of vasoactive substances including biogenic amines, neuropeptide Y, somatostatin, enkephalin, ACTH, corticotropin-releasing hormone, growth hormone releasing hormone, vasoactive intestinal peptide, calcitonin, and atrial natriuretic factor have been extracted from intra-adrenal and extra-adrenal pheochromocytomas in men. Some of them appear to play an important role for the development of hypertension or clinical serious symptoms. However, informations on the molecular forms of other substances in pheochromocytomas are still limited, and precise amount of the peptides or hormones in the tumors has not yet been quantitated. Numerous in vitro or in vivo studies of this documented neoplasm over the years have been reviewed in this manuscript. Clinical analyses of early diagnosis, localization diagnosis, treatment of multiple endocrine neoplasia, preoperative and operative treatments are also evaluated in this paper. These informations will probably provide additional evidence for the multi-secretory APUD cells of neural crest origin and will contribute the therapy in patients with pheochromocytoma.
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PMID:[Pheochromocytoma--basic and clinical analyses]. 134 92

The aim of this study was to investigate the effect of in vivo estrogen administration on hypothalamic growth hormone releasing hormone (GHRH) and somatostatin (SS) gene expression. We found that estrogen administration (estradiol valerate 250 micrograms/every 3 days, subcutaneously) to male rats induced a decrease in both hypothalamic GHRH mRNA levels and GHRH content, that was significant after 3 and 8 days of treatment. In contrast SS mRNA levels were transiently elevated after 1 and 3 days of estrogen administration, returning to normal values after 8 days of treatment. These data suggest that the existence of sexual dimorphism in GH secretion in the rat could be mediated to some extent by gonadal hormones regulating somatostatin and GHRH gene expression in the hypothalamus.
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PMID:Differential effects of in vivo estrogen administration on hypothalamic growth hormone releasing hormone and somatostatin gene expression. 135 46

The 24-h growth hormone secretory pattern and GH response to growth hormone releasing hormone, the alpha 2-adrenoceptor agonist clonidine and the somatostatin-analogue SMS 201-995 were evaluated in 9 patients with Alzheimer's disease and 9 age- and body body-matched control subjects. The secretory profile did not differentiate between patients and controls. Both secreted the largest amount of GH during the early nighthours between 22.00-02.00, whereas the majority of daytime GH levels were below the assay's detection limit (0.4 ng/ml). No difference was found in GH response to GHRH between patients and controls. All subjects showed significantly enhanced GH secretion after GHRH. Dividing the patients into two groups according to age-of-onset (less than 60 years greater than), there was a trend toward larger GH responses to GHRH for the early-onset group. No other parameter differentiated the groups. GH levels after clonidine were blunted in all subjects but one AD patient, probably due to an age-dependent attenuation frequently observed in subjects over 45 years of age. Finally, the administration of the somatostatin-analogue did not render conclusive results, since spontaneous decline of GH concentration was already beginning 2 hours before the drug was given and continued steadily throughout the observation period. In conclusion, patients with only mild to moderate degree of Alzheimer's disease have no prominent changes in GH regulation.
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PMID:Growth hormone secretion in Alzheimer's disease: 24-hour profile of basal levels and response to stimulation and suppression studies. 152 42

The effects of intravenous (IV) and intracerebroventricular (ICV) administration of either bovine growth hormone releasing hormone (GRF) or thyrotrophin releasing hormone (TRH) on plasma growth hormone (GH) and glucose levels have been examined in sheep. Intravenous GRF 1-29NH2 at 3 and 30 micrograms stimulated an increase in GH levels in a dose-dependent fashion; administration of GRF into a lateral cerebral ventricle, however, produced a smaller GH response which was similar at these two doses. Evaluation of somatostatin levels in petrosal sinus blood (which collects pituitary effluent blood) showed that ICV administration of GRF stimulated a release of somatostatin into the blood. Furthermore, concurrent administration of GRF and a potent anti-somatostatin serum ICV resulted in a much enhanced release of GH which was similar to that obtained with a comparable dose of GRF given IV. TRH (as another putative GH-secretagogue) was also administered both IV and ICV. When given IV, 200 micrograms (but not 100 micrograms) TRH produced an elevation in GH levels. By contrast, when 5 micrograms TRH was given ICV there was a decrease in circulating GH levels, but no change in plasma somatostatin concentrations. These results indicate that the smaller GH response to ICV- compared with IV-administered GRF is due to the release of somatostatin within the brain. In addition, it would seem that TRH is not a physiological GH-secretagogue in sheep.
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PMID:Neuroendocrine regulation of growth hormone secretion in sheep. V. Growth hormone releasing factor and thyrotrophin releasing hormone. 161 57

The effects of streptozotocin diabetes on the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA was measured in control rats, in diabetic rats maintained on insulin, and in diabetic rats in which insulin had been withheld for 3 days. Total cytoplasmic RNA samples were prepared from the pituitary and hypothalamic tissues of each animal and analyzed by dot blot or Northern blot hybridization. No significant difference was observed between control and insulin-treated groups with regard to body weight or plasma glucose concentration. The insulin withdrawal group had significantly higher plasma glucose concentrations and lower body weights, confirming diabetic status. There was no significant difference in the level of growth hormone, growth hormone releasing hormone, and somatostatin mRNA among any of the three groups however. We conclude that alterations in the regulation of circulating growth hormone in the streptozotocin-induced diabetic rat, removed from insulin treatment for 3 days, did not occur at the transcriptional or RNA processing level. This conclusion extends to hypothalamic growth hormone releasing hormone, and somatostatin gene expression as well. Regulatory changes in growth hormone level previously noted during insulin withdrawal in the streptozotocin-induced diabetic rat could be the result of post-transcriptional processes operating at the level of hormone synthesis or release.
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PMID:Expression of growth hormone, growth hormone releasing hormone, and somatostatin genes is unperturbed in the streptozotocin-induced diabetic rat. 168 55

Somatostatin (SRIF) reduces growth hormone releasing hormone (GRF)-stimulated growth hormone (GH) release from avian and mammalian adenohypophyseal cells. The present studies examined the intracellular mechanisms mediating SRIF inhibition of GRF-stimulated GH release from chicken pituitary cells. Increases (P less than 0.05) in GH release were observed in the presence of (1) GRF; (2) the adenylyl cyclase stimulator, forskolin; (3) a cAMP analog, 8-bromo-cAMP; (4) the phosphodiesterase inhibitor 3-isobutyl-l-methyl-xanthine (IBMX) combined with GRF; (5) a tumor-promoting phorbol ester and protein kinase C activator, phorbol 12-myristate, 13-acetate (PMA); (6) a diacylglycerol analog, 1,2-dioctanoyl-glycerol (DiC8); and (7) a calcium ionophore, A23187, alone and in combination with PMA. Somatostatin (10 ng/ml) reduced the release of GH stimulated by GRF, forskolin, and 8-bromo cAMP and the GRF-provoked release of GH in the presence of IBMX (P less than 0.05). Somatostatin, however, did not influence GH release in the presence of the protein kinase C activators, PMA or DiC8, or the calcium ionophore A23187. These data suggest that SRIF inhibits GRF-provoked GH release by reducing the ability of the cAMP-protein kinase A but not of the calcium or protein kinase C intracellular message pathways to stimulate GH release.
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PMID:Possible involvement of adenylyl cyclase-cAMP-protein kinase a pathway in somatostatin inhibition of growth hormone release from chicken pituitary cells. 170 26

To determine the effects of prepubertal ethanol (ETOH) exposure on hypothalamic and pituitary hormones known to be involved in the onset of female puberty, we have chronically exposed female rats to either a liquid-diet containing ETOH or an isocaloric control liquid-diet. An additional set of controls consisted of animals maintained on Lab Chow, and water provided ad lib. Our results indicate that the feeding regimen employed produced no differences with regard to body and reproductive organ weights, as well as any of the hormones measured between the two control groups. Conversely, ETOH-treated animals showed significantly lower body and reproductive organ weights than the control animals and although no differences were detected between ETOH-treated and control animals with regard to the hypothalamic content of somatostatin (SRIF), there was a significant increase in the hypothalamic content of growth hormone releasing hormone (GHRH), with a concomitant and significant decrease in the serum concentration of growth hormone (GH). Furthermore, the ETOH-treated animals showed a significant increase in the hypothalamic content of luteinizing hormone releasing hormone (LHRH) with a significant decrease in the serum concentration of luteinizing hormone (LH), but not follicle stimulating hormone (FSH). These results demonstrate for the first time that chronic, prepubertal ETOH administration alters the concentrations of specific hypothalamic and pituitary hormones which are known to be involved in the female pubertal process.
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PMID:Actions of ethanol on hypothalamic and pituitary hormones in prepubertal female rats. 196 48

Following a standard mixed meal, plasma concentrations of growth hormone releasing hormone (GHRH), somatostatin (SMS) and growth hormone (GH) were measured every 30 min for 300 min in six young adults with type I insulin-dependent diabetes mellitus (IDDM) and five normal controls. Mean blood glucose concentrations were higher and mean free insulin levels lower in the diabetics compared with controls both in fasting specimens and at all times following the mixed meal. Basal concentrations (mean +/- SEM) of GHRH were similar in diabetic (12.7 +/- 1.8 pg/ml) and control subjects (11.8 +/- 1.1 pg/ml). Following ingestion of the mixed meal, a rise in GHRH was observed in the control subjects maximal between 30 and 240 min (P less than 0.025) but the response was blunted in the diabetics. Mean GHRH concentrations were greater in the controls than in the diabetic subjects at all stages during the test, the maximum difference being noted at 120 mins (P less than 0.04). Basal SMS concentrations and those observed after the mixed meal were similar in diabetic and control subjects. These results indicate that glucose and insulin may play a role in the regulation of GHRH release following a mixed meal but circulating levels of GHRH and SMS are unlikely to be relevant to the abnormal regulation of GH in IDDM.
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PMID:The growth hormone releasing hormone (GHRH) response to a mixed meal is blunted in young adults with insulin-dependent diabetes mellitus whereas the somatostatin response is normal. 197 74

Neuropeptide Y is found in brain tissue. In dogs it has been shown to enhance activation of the hypothalamic-pituitary-adrenal axis by corticotropin-releasing hormone. It is localized in certain catecholamine neurons and to some extent colocalized with somatostatin. Disturbances of the central noradrenergic system may underlie some forms of alcoholism. Therefore, we compared male alcoholics and normal controls on cerebrospinal fluid (CSF) levels of neuropeptide Y. There was no significant difference between the two groups for neuropeptide Y. There was also no significant difference for CSF levels of growth hormone releasing hormone. However, there were significant positive correlations between CSF levels of neuropeptide Y and CSF levels of corticotropin-releasing hormone, somatostatin, and growth hormone releasing hormone.
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PMID:CSF neuropeptide Y in alcoholics and normal controls. 197 53


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