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)

Effects of various hormonal and pharmacological manipulations on somatostatin distribution were investigated to elucidate the physiological significance of somatostatin in the hypothalamus and the other regions of the rat brain. Immunoreactive somatostatin (IRS) was measured by radioimmunoassay newly developed. Insulin induced an increase of hypothalamic IRS and a decrease of plasma RGH, while glucose administration resulted in the opposite responses, which were not significant. Insulin also increased IRS in the thalamus and the brain stem. The insulin-induced increase of hypothalamic IRS was reduced by hyperglycemia. Glucagon reduced IRS initially and then increased it with an elevation plasma RGH. L-dopa did not affect hypothalamic IRS, although it decreased plasma RPRL. Phentolamine slightly increased plasma RGH and decreased IRS in most regions of the rat brain, while propranolol increased IRS in these regions. Pretreatment with propranolol significantly increased plasma RGH 120 min after insulin administration, and hypothalamic IRS decreased initially by pretreatment with propranolol, and then it increased significantly. When pretreated with propranolol, glucagon markedly increased plasma RGH and decreased IRS significantly. From these findings it is concluded that hypothalamic IRS may participate in the hormonal regulatory system in correlation to plasma RGH, as observed in studies on plasma GH and hypothalamic IRS following insulin, glucose, propranolol or phentolamine administration, but IRS in other regions of the brain may have some other actions as a neurotransmitter or a modulator, because of no significant correlation between plasma GH or PRL and IRS in these regions following various stimuli. In addition, glucose homeostasis and adrenergic mechanism may be important factors in regulating IRS in the rat brain.
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PMID:Immunoreactive somatostatin in the hypothalamus and other regions of the rat brain: effects of insulin, glucose, alpha- or beta-blocker and L-dopa. 3 44

The effect of a sulfonylurea, glibenclamide, on the release of insulin, glucagon, and somatostatin was studied in the isolated perfused rat pancreas. At glucose concentrations of 1.1 mM or less, the drug stimulated somatostatin release, whereas glucagon release, after 2-3 min of increase, was markedly inhibited. Insulin release was moderately stimulated, and maximal release occurred relatively late. A moderate glucose load (6.7 mM) inhibited glibenclamide-induced release of somatostatin, whereas the two in combination exerted an additive action on insulin release. Greater glucose loads, which by themselves would stimulate somatostatin release, only marginally suppressed glibenclamide-induced somatostatin release. The insulinogenic effect of these glucose levels was not modified by glibenclamide. Glibenclamide may thus stimulate both the alpha and beta as well as delta cells of the pancreas, depending on glucose concentration. We suggest a paracrine (local) interaction of somatostatin with the alpha and beta cells, which has an important role in the kinetics of insulin and glucagon release induced by sulfonylureas.
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PMID:Effect of glucose/sulfonylurea interaction on release of insulin, glucagon, and somatostatin from isolated perfused rat pancreas. 11 58

Insulin-, glucagon-, and somatostatin-containing cells were evaluated by morphometry in sections of pancreas treated for immunofluorescence. Glucagon- and somatostatin-containing cells were found to be increased in islets of streptozotocin-diabetic rats as compared to control islets.
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PMID:[Activity of somatostatin-containing cells of the Ilets of Langerhans in experimental diabetes]. 13 Sep 91

Insulin-, glucagon-, and somatostatin-contianing cells, identified by immunofluorescent staining, were quantitated morphometrically in sections of pancreas obtained from diabetic and nondiabetic humans and rats. Both the volume density and number of somatostatin- and glucagon-containing cells were significantly increased in the islets of juvenile-type human diabetics and of streptozotocin diabetic rats.
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PMID:Hypertrophy and hyperplasia of somatostatin-containing D-cells in diabetes. 13 13

By the enzyme-labeled antibody method, cells containing somatostatin (SRIF) as well as insulin or glucagon were identified in pancreatic islets of the rat. SRIF antiserum was raised in rabbits followin immunization with synthetic SRIF coupled with human serum alpha-globulin and did not cross-react with hypothalamic, pituitary or gastrointestinal hormones using our immunoassay method. In the control rats, SRIF-containing cells were scattered in the periphery of the islets in close proximity to the outer glucagon containing cells. These latter cells were distributed in the outermost periphery of the islets. Insulin-containing cells were located in the central portion of the islets and dominantly occupied most of the islet. In the streptozotocin-diabetic rat, SRIF-containing cells were significantly increased in number whereas insulin-containing cells were markedly reduced. It is suggested from these findings that the number as well as the distribution of SRIF-, insulin- and glucagon-containing cells was important to the physiological and pathophysiological functioning of the islet.
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PMID:Immunohistochemical changes of somatostatin cells in the pancreatic islets of rats after streptozotocin administration. 14 56

In order to study the oeffect of somatostatin on the endocrine pancreas directly, islets isolated from rat pancreas by collagenase were incubated for 2 hrs 1) at 50 and 200 mg/100 ml glucose in the absence and presence of somatostatin (1, 10 and 100 mg/ml) and2) at 200 mg/100 ml glucose together with glucagon (5 mug/ml), with or without somatostatin (100 ng/ml). Immunologically measurable insulin was determined in the incubation media at 0, 1 and 2 hrs. Insulin release was not statistically affected by any concentration stomatostatin. On the other hand, somatostatin exerted a significant inhibitory action on glucagon-potentiated insulin secretion (mean +/- SEM, mu1/2 hrs/10 islets: glucose and glucagon: 1253 +/- 92; glucose, glucagon and somatostatin: 786 +/- 76). The insulin output in th epresence of glucose, glucagon and somatostatin was also significantly smaller than in thepresence of glucose alone (1104 +/- 126) or of glucose and somatostatin (1061 +/- 122). The failure of somatostatin to affect glucose-stimulated release of insulin from isolated islets contrasts its inhibitory action on insulin secretion as observed in the isolated perfused pancreas and in vivo. This discrepancy might be ascribed to the isolation procedure using collagenase. However, somatostatin inhibited glucagon-potentiated insulin secretion in isolated islets which resulted in even lower insulin levels than obtained in the parallel experiments without glucagon. It is concluded that the hormone of the alpha cells, or the cyclic AMP system, might play a part in the machanism of somatostatin-induced inhibition of insulin release from the beta-cell.
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PMID:Somatostatin-induced inhibition of insulin secretion from isolated islets of rat pancreas in presence of glucagon. 16 38

An insulin-producing islet cell tumor of the Syrian hamster has been studied in vitro for its capacity to respond to known stimuli of insulin release. Insulin secretion during short term incubation and perifusion of fragments of tumor was detected by radioimmunoassay. Insulin release was increased 2-4 fold by 40 mM potassium in the presence of calcium, glucose (22 mM), glucagon (0.3-3.0 muM), N6,02'-dibutyryl adenosine 3',5'-monophosphate (cAMP; 6mM), and theophylline (10 mM). Concentrations of glucagon that induced insulin release were also effective in activating adenylate cyclase in the membranes of tumor cells. Thus, this tumor appears to possess a cAMP-mediated mechanism for insulin release. Somatostatin (0.8-25 mum) inhibited glucagon-induced insulin release without altering basal or glucagon stimulated adenylate cyclase activity. It would appear that inhibition of glucagon induced insulin release by somatostatin is not mediated by adenylate cyclase. We propose that insulin release by this tumor is sufficiently similar to that found in normal islets so as to make it a suitable model for biochemical studies that require large quantities of homogeneous tissue.
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PMID:Regulation of in vitro insulin release from a transplantable Syrian hamster insulinoma. 16 25

A human pancreatic beta cell tumor was maintained in monolayer cell culture for 80 days. The culture was terminated because of bacterial infection. Probably because extensive trypsin-collagenase dissociation was unnecessary, the dissociated cells attached much more quickly to the surface of the culture flask than do rat pancreatic cells obtained by enzymatic dissociation. Insulin release not only oscillated widely during the first 40 days of culture but also showed a decline from 380 mU the first week to about 50 mU/week the seventh week. For some unknown reason fibroblast overgrowth was not a major problem. Reduction of the medium glucose concentration from 16.5 mM to 5.5 mM did not alter insulin release rate. At glucose concentration of 16.5 mM, somatostatin 1.0 mug/ml reduced insulin release by 40%. From our previously reported studies on the effect of somatostatin on insulin release by monolayer cell cultures of rat endocrine pancreas, we conclude that the constant release of insulin by the tumor cells is relatively nonstimulated. We have confirmed that monolayer cultures of human pancreatic beta cell tumor do not represent a good model for normal human beta cell function because of the major shortcoming of an apparent inability to recognize glucose as a secretogogue.
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PMID:Monolayer cell culture of human pancreatic beta cell tumor: effect of glucose and somatostatin on insulin release. 17 3

Insulin release in the perfused isolated rat pancreas was measured after stimulation with 16.5 mM glucose with and without somatostatin (cycle form, 100 ng/ml) in the medium. A complete blockage of the typical biphasic pattern of insulin release ocurred with somatostatin in the medium. Such blockage was abolished when cAMP (2.5 mM) and a 0.5 ml solution of glucagon (1 mg/ml) were continuously perfused for 20-minute periods and for 30-second periods correspondently. It did not take place when glibenclamide (HB-419) was perfused for a 20-minute period at a rate of 10 mug/ml. The results suggest that the adenylcyclase dependent mechanisms of glucose-induced insulin release are involved in the inhibition of the glucose-induced insulin secretion by somatostatin.
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PMID:Inhibition of the glucose induced insulin release by somatostatin in the isolated perfused rat pancreas. Action of cyclic AMP, glucagon and glibenclamide. 18 68

A number of enzymatic methods have been developed to prepare hepatocytes using collagenase and hyaluronidase. However, best cell preparations are obtained by using only low concentrations of collagenase and exposing the liver to the enzyme for a very short period of time. These isolated cells with intact cell membranes and large numbers of microvilli on the cell surface respond to hormones at physiological concentrations suggesting that these microvilli contain hormone receptors. In addition, high glycogen content is essential to maintain the in vivo metabolic characteristics of the hepatocytes suggesting that intracellular glycogen plays an important role in the hormonal regulation of metabolism in hepatocytes. Studies with glucagon and insulin on carbohydrate metabolism show that the molar ratios of these hormones control gluconeogenesis and glycogenolysis. Furthermore, in vitro addition of insulin stimulates glycogen synthesis and activates glycogen synthase. Insulin also stimulates protein synthesis in cells containing high glycogen and maintains more normal parallel strands of polyribosomes. Studies with isolated hepatocytes from diabetic, hypophysectomized and adrenalectomized animals show a reduced glucagon response to glycogenolysis. This lack of glucagon response was not due to reduction in glycogen levels. Other hormones such as somatostatin and parathyroid also give rise to alterations in carbohydrate metabolism in isolated hepatocytes.
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PMID:Studies of hormonal regulation of metabolism using isolated hepatocytes. 19 66


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