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)

The purpose of this study was to delineate the possible endocrine effects of exercise-induced GH secretion. Twelve healthy adult males were studied during short (20 min) and subsequent prolonged (2 h) physical exercise and recovery period (2 h), both after injection of a long acting somatostatin analog [Sandostatin (ST); 0.1 or 0.05 mg, sc] and after a control saline injection. Additional subjects were studied during rest with similar injections of ST (0.1 mg) and saline (n = 7) or using a lower ST dose (0.01 mg; n = 6). Several venous blood samples were taken during the trials and analyzed for selected hormones, monitoring pituitary, testicular, and adrenal functions. ST injection blocked the serum GH response to short term maximal bicycle ergometer exercise, but not to the following prolonged bicycle exercise. No relationship of the exercise-associated GH increase to the concomitant endocrine responses of the adrenals and testes was observed. Unexpectedly, the higher ST doses (0.1 and 0.05 mg) increased the mean levels of serum testosterone by 18-25% in both exercise (P = 0.0017) and rest trials (P < 0.0001), respectively. ST did not affect the levels of LH, FSH, or cortisol. ST slightly increased serum sex hormone-binding globulin (3%; P = 0.021) and albumin (4%; P = 0.017) concentrations, but not that of free testosterone. Because the testosterone response to somatostatin was fast and without a simultaneous increase in LH, it was consistent with a direct testicular response. The explanation for this novel ST effect remains obscure, but it may be due to modulation of some paracrine mechanisms inhibiting testicular steroidogenesis.
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PMID:Effects of a long acting somatostatin analog on pituitary, adrenal, and testicular function during rest and acute exercise: unexpected stimulation of testosterone secretion. 759 42

The hypothalamo-pituitary-gonadotrophic axis develops in the sheep fetus from midgestation to late gestation. The GnRH neuronal centres seem to be fully developed in the fetus and their localization complies with the adult pattern. Pituitary gonadotrophs are responsive to exogenous GnRH and release LH and FSH in a pulsatile fashion; the highest concentrations in plasma are found during late gestation. In sheep, maturational changes of this axis continue through to the prepubertal period. The GnRH neuronal system is established at about 12 weeks of age. The pattern of LH and FSH release is characteristic for each gonadotrophin depending on age and sex. The responsiveness of the gonadotrophs to GnRH increases up to 3 weeks of age. It is concluded that the changes in morphology and physiology of the hypothalamo-pituitary-gonadotrophic axis reflect the progressive maturation of the central mechanisms involved in the control of gonadotrophin secretion throughout fetal and prepubertal growth in sheep. Development of the hypothalamo-pituitary-somatotrophic axis begins in the fetus around mid-gestation. The central regulation of growth hormone (GH) in the fetus probably has a dual character, although the growth hormone releasing hormone (GHRH) neuronal system has not yet been observed in sheep. The somatostatin neuronal system develops in diverse neuronal centres in the fetus. The somatostatin centre involved in hypophysiotrophic functions does not develop fully before birth and is established over the first 10 weeks after birth. Plasma GH concentrations are very high in the fetus and fall suddenly in the perinatal period, and after a temporary increase they decline with age.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of the gonadotrophic and somatotrophic axes of sheep. 762 13

In the past, pituitary tumours that produce one or more of the glycoproteins (TSH, LH, FSH and alpha subunit) were thought to be rare. However, using modern immunocytochemical and molecular biology techniques, these tumours are being recognized with increasing frequency. Many of these tumours produce glycoprotein alpha and beta subunits in addition to intact glycoproteins. Hormone production is often low compared with tumour size, and serum hormone levels may not be elevated in these patients. Tumours that produce the gonadotrophins (LH or FSH) or alpha subunit account for the majority of clinically non-functioning pituitary adenomas. They do not cause a specific clinical syndrome, and usually present with symptoms of a large mass lesion and/or hypopituitarism. Optimal treatment of these tumours is often difficult. The initial approach is usually transsphenoidal surgery, followed by radiation therapy if there are symptoms due to residual tumour. Medical therapy of gonadotrophin and alpha subunit tumours may include the use of dopamine agonists or somatostatin analogues, although neither has been shown to consistently decrease tumour size. Preliminary trials with experimental GnRH antagonists suggest that these agents may be useful as adjuvant therapy of gonadotrophin tumours. Tumours that produce TSH are rare. Patients present with hyperthyroidism, which is often misdiagnosed as Graves' disease, as well as with symptoms of a pituitary mass lesion. Almost all TSH tumours secrete excess amounts of free alpha subunit. Optimal treatment of these tumours includes transsphenoidal surgery, followed by radiation therapy for residual tumour. The somatostatin analogue octreotide is effective in reducing excess TSH secretion from these tumours, and causes a reduction in tumour volume in a significant minority of patients.
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PMID:Glycoprotein-secreting pituitary adenomas. 762 88

At present, four main types of serotonin (5-HT) receptors have been identified in the brain (5-HT1, 5-HT2, 5-HT3, and 5-HT4). In addition, the 5-HT1 have been further subclassified. We have taken advantage of a new selective 5-HT1D receptor agonist 3-[2-(dimethylamino)ethyl]-N-methyl-1H-indole-5-methanesulfonamide succinate, Sumatriptan, to evaluate the role of 5-HT1D receptors on GH secretion. To this end, several tests with or without sumatriptan were undertaken in normal prepubertal children. Furthermore, we assessed the effect of Sumatriptan on basal GH secretion and the GH response to GHRH in obese children. In normal children, Sumatriptan administration (3 mg, sc) resulted in an increase in basal GH levels at 30 min (7.7 +/- 1.5 micrograms/L; P < 0.05) and increased GH responses to GHRH (47.3 +/- 6.4 vs. 29.6 +/- 9.7 micrograms/L; P < 0.05). The Sumatriptan-induced increase in GH responses to GHRH was dependent on the stimulus tested. Pretreatment with Sumatriptan did not modify the GH response to clonidine or pyridostigmine, as assessed by the peak GH response and the area under the curve. In contrast, it increased the GH response to arginine. In the obese subjects, the GH response to GHRH was reduced (7.3 +/- 1.0 vs. 29.6 +/- 9.7 micrograms/L at 30 min) compared to that in control children (P < 0.05). Sumatriptan administration did not alter the basal GH value (peak GH, 1.7 +/- 0.3 micrograms/L at 30 min). However, Sumatriptan administration clearly increased the effect of GHRH, resulting in a GH peak of 14.6 +/- 3.1 micrograms/L at 30 min (P < 0.01). To assess the specificity of Sumatriptan on anterior pituitary hormone secretion, we studied its effect on TSH and PRL responses to TRH as well as LH-releasing hormone-induced LH and FSH secretion. Administration of Sumatriptan did not alter the response of any of these hormones. Our results indicate that 5-HT1D receptors have a stimulatory effect on GH secretion, possibly by inhibiting hypothalamic somatostatin release.
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PMID:Role of the serotonin receptor subtype 5-HT1D on basal and stimulated growth hormone secretion. 777 48

The factors that determine the hormone and volume responses of pituitary adenomas to the somatostatin analog octreotide are poorly understood. We, therefore, studied the correlation between 111indium-pentetreotide somatostatin receptor scintigraphy (SRS) and the clinical and immunohistochemical classification of pituitary adenomas, on the one hand, and hormone and volume responses, on the other hand. Ten patients with GH-secreting (6 females and 4 males; age, 31-67 yr) and 14 patients with clinically nonfunctioning (NF) macroadenomas (5 females and 9 males; age, 22-79 yr) were preoperatively treated with 300 micrograms/day octreotide, which was increased to 600 and 1500 micrograms/day at weekly intervals and then continued for at least 3 months until surgery. SRS was performed before therapy. A sellar magnetic resonance imaging scan was performed before therapy; 1, 2, and 3 weeks and 3 months after start of therapy; and after surgery. Acromegalics also had an 8-h GH profile, insulin-like growth factor-I determination, and a 100-g oral glucose load at these time points. An attempt was made to identify NF adenomas as gonadotroph adenomas using their LH, FSH, and alpha-subunit responses to TRH. In acromegalic patients, octreotide suppressed mean GH (8-h profile) and insulin-like growth factor-I concentrations from 34.9 +/- 9.7 to 8.1 +/- 3.6 micrograms/L and from 2122 +/- 1025 to 701 +/- 208 micrograms/L, respectively, after 3 months. Significant (26-85% decline) tumor shrinkage occurred in 5 of 10 patients, mainly within the first week. Tumor shrinkage and GH suppression were not correlated. Four of 7 patients had increased pituitary 111indium-pentetreotide uptake, but this did not predict GH suppression or tumor shrinkage. Of the NF adenomas, 2 responded with shrinkage (57% and 96% decline). Four of 12 adenomas had increased 111indium-pentetreotide uptake, but this did not correlate with tumor shrinkage (2 adenomas; 1 gonadotroph and 1 null cell adenoma), immunohistochemistry, or clinical classification. We conclude that preoperative octreotide therapy suppresses GH in most patients and reduces tumor volume in up to 50% of acromegalic patients. It also induces shrinkage in some NF adenomas, although less frequently. SRS does not predict shrinkage of either tumor type. Shrinkage does not correlate with clinical classification or immunohistological characteristics. Further studies are needed to identify the factors that determine the hormone and volume responses of pituitary adenomas to octreotide therapy.
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PMID:Preoperative octreotide treatment of growth hormone-secreting and clinically nonfunctioning pituitary macroadenomas: effect on tumor volume and lack of correlation with immunohistochemistry and somatostatin receptor scintigraphy. 796 37

Five patients with gonadotropin-secreting pituitary adenomas were studied. The utility of gonadotropin response to TRH stimulation in the diagnosis and follow-up of these tumors was evaluated, as well as the effects of somatostatin analogue SMS 201-995 and bromocriptine on gonadotropin release. Three patients had FSH and LH secreting adenomas while the other two tumors secreted FSH and alpha-subunit. Transsphenoidal resection of the pituitary adenomas were performed in all patients. Following preoperative TRH administration (400 micrograms i.v.), marked increases were observed in FSH levels in two cases, in LH levels in three and in alpha-subunit in one. The FSH and LH responses to t.his stimulus persisted in the same patients after surgery. Following acute bromocriptine administration (5 mg orally), FSH was reduced in all cases by 19% to 46%, LH in three cases by 50-67% and alpha-subunit in one by 33%. In patient no. 5, with persistent high FSH levels in the immediate postoperative period, long-term bromocriptine treatment was administered (15 mg/d orally), resulting in normalization of FSH levels 6 months later, although the size of the tumor was not reduced. After acute SMS 201-995 administration (100 micrograms sc) FSH decreased in two cases by 38% and 76%, LH in three by 30-56% and alpha-subunit in one by 20%. We conclude that gonadotropin response to TRH stimulation is useful in the diagnosis and follow-up of patients with gonadotroph adenoma. Bromocriptine and SMS 201-995 may be effective as coadjuvant treatment following surgery and radiotherapy in these patients, although long-term studies will be necessary to confirm these proposals.
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PMID:Usefulness of thyrotropin-releasing hormone test, SMS 201-995, and bromocriptine in the diagnosis and treatment of gonadotropin-secreting pituitary adenomas. 800 39

1. The sympathetic superior cervical ganglia (SCG) provide innervation to the pineal gland and median eminence through the internal carotid nerve and to the thyroid and parathyroid glands through the external carotid nerve. 2. Postsynaptic activation in median eminence nerve endings shortly after superior cervical ganglionectomy (SCGx) was accompanied by a depression of LH and FSH release and by a 3-5 day delay in rat estrous cyclicity. A decrease in TSH and GH release and an increase in ACTH and prolactin release were also found. These effects were accompanied by a) an increase in medial basal hypothalamic (MBH) LHRH, TRH and GHRH, b) a decrease in MBH somatostatin, AVP and CRH, and c) a normal adenohypophyseal response to hypophysiotropic hormones. Neurohypophyseal AVP release decreased during degeneration of sympathetic nerve terminals in the neurohypophyseal lobe after SCGx. The effects were generally mediated by alpha 1-adrenoceptors and were pineal gland. 3. In thyroid and parathyroid tissue the following events were observed during the wallerian degeneration phase after SCGx: a) alpha 1-adrenoceptor inhibition of thyroxine (T4) release, b) alpha 1-adrenoceptor inhibition, together with beta-adrenoceptor stimulation, of calcitonin release, and c) alpha 1-adrenoceptor inhibition of parathyroid hormone release. Thyroid sympathetic nerves also modulate slow phenomena such as compensatory thyroid growth after partial thyroidectomy. 4. In rats subjected to cholinergic decentralization of the thyroid gland, a decrease of plasma T4 and an increase of plasma TSH, as well as an impaired goitrogenic and thyroid compensatory response were detectable. The calcitonin and PTH response to changes in calcium levels increased after regional parasympathetic denervation. 5. The results indicate that cervical autonomic nerves constitute a parallel pathway through which the brain communicates with the endocrine system.
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PMID:Peripheral neuroendocrinology of the cervical autonomic nervous system. 808 Dec 83

Insulin, glucagon, somatostatin, and PP cells were found by immunotopochemical and electron-optical techniques in the islets of Langerhans of the sand rat, proving that the islets in this species also contain the four basic cell types known to be found in the islets in mammals in general. The ratio of A cells to B cells was 1:4 (19.1% A cells to 80.9% B cells). The pancreas of the sand rat contained assemblages of various numbers of neurons in the intralobal and interlobular connective tissue. They did not seem related in any regular fashion to specific blood vessels or branches of the pancreatic ducts. No bundles of nerve fibers were found by either light or electron microscopy. Nonmyelinated nerve fibers were detected by electron microscopy in the stroma of the islets. In the sand rat the neuroinsular complexes are formed by the penetration of single nerve cells into the pancreatic islets. In the NH or long-term group the islets exhibited signs of stimulation. The number of islets was higher than normal (polynesia), with the islets themselves enlarged (macronesia). Double islets in the secretory ducts of the exocrine pancreas were frequent. The increase in islet size was due to hyperplasia of the B cells. The numbers of beta-granules in the B cells varied considerably. Glycogen was demonstrated in some islets. The fusion of beta-granules was shown in electron microscopic pictures. The electron-opaque centers of these granules were brighter than the others and appeared to have partly dissolved. The organelles of the B cells (ER, Golgi apparatus, and mitochondria) were well developed, this also being a sign of cell stimulation. No changes were observed in the B and PP cells. Stimulation of the islet cells was even more pronounced in the diabetic group. Due to hyperplasia, the islets in this group were significantly larger not only than those in the control group, but also than those in the NH group. The pancreata of this group of sand rats contained numerous small islets. Although necrotic B cells were found in the large islets of the pancreas, none were discovered in the small islets. The small islets were considered to be "regenerated" islets. Granulation was slight in the remaining functioning B cells. The hypophyses of the control group contained the GH, LTH, FSH, LH, and TSH cell types typical of this organ in other species. In the sand rat the granules of these cell types are of about the same size as has been stated for other rodents.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Histophysiology of the obesity-diabetes syndrome in sand rats. 808 78

To evaluate the significance of endogenous vasopressin and oxytocin in control of anterior pituitary hormone release, antiserum against vasopressin (AB-VP) or oxytocin (AB-OT) were microinjected into the third ventricle (3V) of conscious, ovariectomized rats to immunoneutralize endogenous VP or OT, respectively. Blood samples were collected just before and at different times after the microinjections. There were no differences in the plasma LH, FSH, PRL and TSH concentrations between control groups injected into the 3V with normal rabbit serum (NRS) and groups submitted to the intraventricular injection of AB-OT or AB-VP for 24 h after the injections. Plasma growth hormone (GH) declined significantly by 4 h after NRS injection, remained low at 6 h and had rebounded to nearly initial levels at 24 h. This pattern was not changed by microinjection of AB-VP, but plasma GH increased significantly compared to initial values in the period from 1 to 24 h after intraventricular microinjection of AB-OT. The intraventricular injection of AB-VP or AB-OT significantly decreased plasma ACTH; however, the effect of AB-VP was more prolonged and persisted for 6 rather than 4 h after injection. Thus, endogenous oxytocin may play a role in the control of basal GH release probably by stimulating somatostatin secretion and/or inhibiting GH-releasing hormone secretion or by both actions. On the other hand, both endogenous vasopressin and oxytocin play a physiologically significant stimulatory role in the control of basal ACTH release.
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PMID:Actions of endogenous vasopressin and oxytocin on anterior pituitary hormone secretion. 839 22

To date, very few studies on the effect of somatostatin on female reproductive function have been reported. In our study, we examined the effects of somatostatin on (i) androgen biosynthesis using whole ovarian dispersates, and (ii) aromatase activity and progesterone production using granulosa cells. Whole ovarian dispersates obtained from immature rats were cultured for 96 h in serum-free medium with human chorionic gonadotrophin (HCG; 25 ng/ml) and insulin (10 micrograms/ml) in the presence or absence of an increasing concentration of somatostatin (0.03-3.00 ng/ml). HCG- and insulin-stimulated accumulation of androsterone by these cells was inhibited significantly by somatostatin. Granulosa cells from diethylstilbestrol-treated rats were cultured for 48 h in serum-free medium with follicle-stimulating hormone (FSH; 20 ng/ml) and FSH plus insulin (1 microgram/ml) with or without somatostatin (0.03-3.00 ng/ml). Both aromatase activity and progesterone production stimulated by FSH and FSH plus insulin were significantly inhibited by somatostatin. Somatostatin by itself (1 ng/ml) did not have an effect on any of the evaluated parameters. The action of somatostatin could be immunoneutralized and did not influence the plated viable cell mass. These findings indicate that somatostatin can regulate ovarian steroidogenesis by mediating gonadotrophin and growth factor action on different ovarian cell types.
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PMID:Somatostatin action on rat ovarian steroidogenesis. 856 24


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