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)

In a continuation of our studies on the mechanism of central nervous system induced hyperglycemia in the rat, we evaluated the relative contribution of a direct neural effect on the liver and of certain hormones to the hyperglycemia induced by administration of thyrotropin-releasing hormone (TRH). The findings were compared with those of a previous investigation using neostigmine or 2-deoxy-D-glucose. In the present study TRH was injected into the third cerebral ventricle of rats, and the concentrations of hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine, were measured. Four groups of animals were evaluated: (1) intact rats; (2) rats receiving an infusion of somatostatin with insulin via the femoral vein to inhibit glucagon secretion and to maintain the basal insulin level; (3) rats bilaterally adrenalectomized (ADX) to prevent epinephrine secretion, and (4) ADX rats administered an infusion of somatostatin and insulin. Evaluation of the areas under the glucose curves for the rats receiving somatostatin with insulin, ADX rats, and ADX rats receiving somatostatin with insulin showed values 202, 50, and 79% of those observed in intact animals. These observations suggest that TRH-induced hyperglycemia results from at least two effects: a direct neural effect on the liver including a suppressive effect of epinephrine on insulin secretion (contributing about 79% to the total hyperglycemic effect) and a direct effect of epinephrine on the liver (contributing about 21% to the total hyperglycemic effect).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relative contribution of nervous system and hormones to hyperglycemia induced by thyrotropin-releasing hormone in fed rats. 168 38

We previously reported that neostigmine injected into the third cerebral ventricle stimulated adrenal secretion of epinephrine, secretion of glucagon from the pancreas, and direct neural innervation of the liver, resulting in hepatic venous plasma hyperglycemia in anesthetized fed rats. However, receptor type of these 3 mechanisms is not known. Therefore, we examined the effects of intraventricularly injected cholinergic or adrenergic antagonists on neostigmine-induced catecholamines in intact rats, glucagon secretion which is mediated by direct neural innervation of pancreas in bilateral adrenalectomized (ADX) rats, and hepatic venous hyperglycemia which is mediated by direct neural innervation of liver in ADX rats receiving constant infusion of somatostatin from femoral vein. Atropine injected into the third cerebral ventricle suppressed epinephrine secretion and dose-dependently inhibited hepatic venous hyperglycemia induced by neostigmine in intact rats. The neostigmine-induced glucagon secretion which occurs in ADX rats was suppressed by atropine. Atropine also prevented the neostigmine-induced hyperglycemia in ADX rats receiving constant somatostatin infusion through femoral vein (ADX-Somato rats). On the other hand, phentolamine, propranolol and hexamethonium showed no significant inhibitory effect on neostigmine-induced hyperglycemia, epinephrine and glucagon secretion in intact rats, glucagon secretion in ADX rats, or hyperglycemia in ADX-Somato rats. These results suggest that neostigmine-induced epinephrine and glucagon secretion and increased hepatic glucose output stimulated by direct neural innervation to liver is mediated by central muscarinic receptor in fed rats.
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PMID:Neostigmine-induced hyperglycemia is mediated by central muscarinic receptor in fed rats. 233 69

We examined the relative contributions of hormones and nervous system to the total 2-deoxy-D-glucose (2-DG)-induced central nervous system-mediated hyperglycemia. 2-DG was injected into the third cerebral ventricle in the following four groups of rats, and hepatic venous plasma glucose, immunoreactive glucagon, immunoreactive insulin, epinephrine, and norepinephrine were measured: 1) intact rats; 2) intact rats receiving somatostatin with insulin infusion through the femoral vein to inhibit glucagon secretion and maintain the basal insulin level; 3) bilateral adrenalectomized (ADX) rats to prevent epinephrine secretion; and 4) ADX rats receiving somatostatin with insulin infusion. Comparing areas under glucose curves among the intact rats, those receiving somatostatin with insulin infusion, ADX rats, and ADX rats receiving somatostatin with insulin infusion, the area under the glucose curve was intact rats greater than intact rats receiving somatostatin with insulin infusion greater than ADX rats receiving somatostatin with insulin infusion greater than ADX rats. These results suggest that there are three distinct sympathetic nervous system responses to 2-DG-induced central nervous system-mediated hyperglycemia. 2-DG-induced hyperglycemia is not dependent on only one of those three systems, it is dependent on all of them. The relative potency of the factors to 2-DG-induced hyperglycemia increases in the following order: direct neural innervation of liver (including suppressive epinephrine action on insulin secretion), glucagon, and direct epinephrine action on liver.
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PMID:The relative importance of nervous system and hormones to the 2-deoxy-D-glucose-induced hyperglycemia in fed rats. 256 82

The populations of endocrine cells in pancreatic islets are subjected to striking fluctuations in their size when subjected to sustained stimulation and/or inhibition of their secretory activity. The stimulation of a specific endocrine secretion is followed by proliferation of its producing cell, a situation that is reversed after interruption or inhibition of the stimulus. Morphometric and cytological modifications of somatostatin and glucagon producing cells (D and A cells respectively) in the islets of Langerhans have been studied by electron microscopy, immunocytochemistry and morphometry in pancreas of rats submitted to the following experimental conditions: 1) Adrenalectomized (ADX), 2) ADX treated with hydrocortisone, 3) Diabetic and 4) Cysteamine (CSH) treated rats. In addition to ultrastructural changes, the populations of A and D cells were analyzed morphometrically applying a computerized system for light microscopy of paraffin sections immunostained with peroxidase-antiperoxidase (PAP) technique. Glucagon cell population displayed striking alterations in fine structural features and in the volume density in the different experimental conditions examined. By contrast, the cytological organization and the size of somatostatin cell population were little or not affected except in the diabetic rats where the massive degeneration of beta cells grossly distorted the structure of the islets. These observations led to the conclusion that the population of D cells constitutes a stable of endocrine system, at variance to the profound modifications occurring in A cells when they are submitted to various experimental conditions that stimulate or inhibit their secretory activity.
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PMID:Differential proliferation of somatostatin and glucagon cells in rat pancreatic islets submitted to various stimuli. 759 19

Steroidogenic enzymes are differentially expressed throughout the ovarian cycle. The complex pattern of cell-specific up- and down-regulation accounts, at least in part, for the cyclic production of estrogens, androgens and progesterone. The gonadotropins follicle-stimulating hormone and luteinizing hormone are the main regulators of ovarian steroid hormone production and act primarily via the cAMP second-messenger system. Previous studies have identified cAMP-responsive sequences (CRS) in a number of genes encoding steroidogenic enzymes. In the present study we attempted to compare the cAMP responsiveness of some of these sequences with each other and with the classical cAMP-response element (CRE), as identified in the somatostatin gene. In addition, we were interested to determine whether or not the information for tissue-specific expression is contained by these sequences. Using transient transfection of reporter gene constructs, comprising the CRS of bCYP11A, bCYP17, hCYP21B and bovine adrenodoxin, we investigated cAMP-dependent and tissue-specific expression in primary cultures of bovine luteal and granulosa cells. Treatment of transfected luteal cells with forskolin markedly increased the expression of all but the CYP17-specific reporter gene constructs. A similar pattern of forskolin responsiveness was observed when these reporter gene constructs were transfected in bovine granulosa cells in primary culture. Furthermore, when a reporter gene construct containing the classical CRE genomic was transfected in bovine luteal cells, its expression was also highly stimulated upon treatment with forskolin. Thus, the classical cAMP/CRE system appears to be functional in these cells. Northern blot analysis of primary cultures of bovine luteal and granulosa cells revealed that bCYP17 and bCYP21B are not expressed in control and forskolin-treated cultures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:cAMP-dependent and tissue-specific expression of genes encoding steroidogenic enzymes in bovine luteal and granulosa cells in primary culture. 839 56

The impact of hypoxia on somatostatin (SS) secretion from the median eminence (ME) of the hypothalamus and the possible glucocorticosteroid involvement in modulating secretion, were investigated in adult male rats exposed to hypoxia. SS levels were measured by specific radioimmunoassay during acute and prolonged hypoxia as well as after bilateral adrenalectomy (ADX) with or without a replacement with dexamethasone (DEX). The results were as follows: (a) acute hypoxia (5 km altitude, 10.8% O(2)) for 2 and 24 h markedly increased SS content in ME, but acute severe hypoxia (7 km, 8.2% O(2) for 24 h) markedly decreased SS level in ME. (b) Chronic hypoxia (10.8% O(2)) from 5 to 25 days exposure did not significantly affect SS content of ME. (c) ADX alone increased SS content of ME and this increase was further enhanced after 2 h exposure to hypoxia. (d) The increased SS in ME of ADX rats was blocked by replacement with DEX (500 microg/rat i.p.). The data presented suggest that acute hypoxia stress may increase or decrease SS content of ME in rats, depending on the severity and duration of the hypoxia and that the stimulatory action of hypoxia on SS content of ME be may in part mediated by the increased corticosterone levels during hypoxia.
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PMID:Hypoxia influences somatostatin release in rats. 1077 21

We reported that hypoxia inhibited the growth hormone (GH) and induced somatostatin (SS) release from the hypothalamic median eminence (ME) of rats. This study is designed to examine the SS mRNA alterations in the periventricular nucleus (PeN) of the hypothalamus in rats and the possible involvement of glucocorticoid (GC) during hypoxia. Rats were exposed to hypoxia in a simulated hypobaric chamber. SS mRNA levels in the PeN were tested by in situ hybridization. Hypoxia of 5-km altitude (10.8% O(2)) for 2, 5 and 24 h increased the SS mRNA expression by 34.72%, 50.31% and 95.05% (p<0.05), respectively. Severe hypoxia of 7-km altitude (8.2% O(2)) enhanced the SS expression by 79.08% (p<0.01), 74.90% (p<0.01) and 71.40% (p<0.05), respectively. Prolonged hypoxia (5 km for 5 days) exposure augmented a 2.5-fold SS mRNA (p<0.001). One week post adrenalectomy (ADX), SS mRNA level was significantly increased. During hypoxia, 5 km for 5 h, SS mRNA in ADX rats was not further increased. An increased SS mRNA was showed by pretreatment with low dose of dexamethasone (DEX) (125 microg/kg, i.p.) to ADX animals but this increase was depressed by a high dose of DEX (500 microg/kg, i.p.). The data suggested that (1) hypoxia stimulated the expression of SS mRNA in the PeN of rat hypothalamus. (2) Increased circulating GC levels might play a role in upregulating the SS mRNA in the rat PeN during hypoxia.
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PMID:Increased somatostatin mRNA expression in periventricular nucleus of rat hypothalamus during hypoxia. 1195 74

Glucocorticoids can differentially regulate somatostatin (SRIH) receptor subtype expression depending on the duration of treatment, dose used and tissue type examined. In order to determine if glucocorticoids are critical regulators of pituitary SRIH receptor synthesis in vivo, we examined the effect of adrenalectomy (ADX), with and without dexamethasone (DEX; 200 microg/day for 8 days) treatment, on the relative expression levels of the SRIH receptor subtypes, sst1-sst5, by multiplex RT-PCR. ADX increased pituitary sst2 mRNA levels, but did not significantly alter mRNA levels of the other SRIH receptor subtypes. These findings indicate that pituitary sst2 synthesis is normally under inhibitory control of endogenous glucocorticoids. High-dose DEX resulted in a decrease in sst1-sst4 mRNA and an increase in sst5 mRNA, independent of adrenal status. DEX also decreased sst2, sst3 and sst4 mRNA levels and increased sst5 mRNA levels by short-term in vitro application (10 nM, 4 h) in primary rat pituitary cell cultures, indicating DEX regulation of sst2-sst5 in vivo is at least in part due to a direct action at the level of the pituitary. However, the inhibitory actions of DEX on sst1 mRNA levels observed in vivo were not consistently replicated in vitro. In order to determine if the somatotrope population of the pituitary would display a similar response to DEX, fluorescent-activated cell sorting was used to obtain somatotrope-enriched cultures (>95% growth hormone immunopositive cells). DEX treatment (10 nM, 4 h) of somatotropes decreased sst2 and sst3, but did not alter sst5 mRNA levels. These results indicate that the effects of DEX on sst5 mRNA levels observed in unsorted pituitary cell cultures might be due to changes in sst5 expression in pituitary cell types other than somatotropes. Since excess glucocorticoids are thought to enhance SRIH tone, we also tested if ligand activation of SRIH receptor subtypes in vitro could mimic any of the actions of DEX on SRIH receptor mRNA levels observed in vivo. To this end, unsorted pituitary cell cultures and somatotrope-enriched cultures were treated with SRIH (1 and 100 nM) for 4 h. SRIH increased sst3 and sst5 mRNA levels, in both culture systems. These results suggest that the DEX-induced increase in endogenous SRIH tone may contribute to enhanced sst5 mRNA levels observed in vivo. However, the stimulatory actions of SRIH on sst3 mRNA levels observed in vitro might be overridden by direct inhibitory actions of DEX.
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PMID:Role of glucocorticoids in the regulation of pituitary somatostatin receptor subtype (sst1-sst5) mRNA levels: evidence for direct and somatostatin-mediated effects. 1451 9