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 current study examines the effects of somatocrinin (GRF) and somatostatin antiserum (ASS) alone and in combination on pancreatic growth. Twenty-four-day-old rats were injected daily s.c. at 10:00 and 16:30 h for 14 days with either saline or GRF (4 and 20 micrograms X kg-1). ASS was given i.p. every other day. Pancreatic weights and DNA, RNA, protein, amylase, and chymotrypsin total contents and concentrations were evaluated at the end of treatment. GRF alone was associated with significant decreases in pancreatic weight and contents of protein, amylase, and chymotrypsin but with significant increases in total DNA content indicating pancreatic atrophy and hyperplasia. ASS alone has a slight effect on DNA content but potentiates GRF given at the dose of 4 micrograms X kg-1. Even though ASS reduced protein and enzyme contents, it prevented the large decreases observed with increasing doses of GRF. These data present for the first time effects of GRF and ASS on pancreatic growth and describe a strong interaction between the two products. It is yet too early to determine how these two substances work on the pancreatic acinar cells, but hypotheses on their possible mode of action are proposed.
Pancreas 1986
PMID:Effect of somatocrinin with or without a somatostatin antiserum on pancreatic growth. 243 58

We studied the effect of four graded doses of SMS 201-995, a synthetic octapeptide somatostatin analogue (27, 80, 240, and 720 ng/kg/h) on the basal and secretin-plus-cerulein-stimulated exocrine pancreatic function and pancreatic polypeptide (PP) release in five healthy volunteers. Duodenal fluid secretion and bicarbonate output under basal and stimulated conditions were not significantly affected by any dose of SMS. The basal and stimulated enzyme secretion were decreased in a non-dose-dependent manner by all SMS doses used in the study and showed a 75% inhibition of the secretin-plus-cerulein-stimulated trypsin and amylase output. The cerulein-stimulated PP release was significantly suppressed by all four SMS doses. SMS appears to be a strong inhibitor of pancreatic enzyme secretion, at the same time affecting the PP release.
Pancreas 1986
PMID:Effect of a new somatostatin analogue on pancreatic function in healthy volunteers. 243 63

In four conscious dogs infusions of glucose (1 g/kg/h) alone or glucose and galanin (2 micrograms/kg/h) were undertaken during cryogenic vagal blockade at -2 degrees C or following atropine (100 micrograms/kg i.v.). When compared to parenteral glucose alone, the addition of galanin substantially elevated plasma glucose and blunted plasma insulin responses. Vagal blockade or atropine failed to alter these effects of galanin on plasma insulin or glucose responses. Moreover, plasma levels of somatostatin, pancreatic glucagon, pancreatic polypeptide, growth hormone, and cortisol were unaffected by galanin infusions. Thus, the inhibition of plasma insulin responses to glucose by galanin is mediated by a nonvagal, noncholinergic mechanism and is independent of changes in either plasma pancreatic glucagon or somatostatin levels. Galanin at the dose employed in the study may have direct and selective actions on the B cell and thus play an important role in the neuromodulation of insulin release.
Pancreas 1988
PMID:Effect of galanin and vagal integrity on insulin release in dogs. 245 71

To study the role of somatostatin in the regulation of pancreatic and gastric functions, a combined isolated rat stomach and pancreas preparation was developed. This model allowed simultaneous measurements of exocrine and endocrine secretion from the pancreas and gastrin secretion from the stomach. Somatostatin was applied either by a linear gradient or by constant infusion with one concentration in the presence of cerulein, secretin, electric vagal activity, or acetylcholine. Somatostatin did not influence exocrine pancreatic secretion irrespective of what substance was stimulated. In contrast, somatostatin significantly inhibited glucose-dependent insulin and gastrin secretion, either basal or stimulated by vagal activity or acetylcholine. Acetylcholine-induced gastrin secretion was more sensitive to inhibition by somatostatin than insulin. We conclude that in an isolated perfused organ system somatostatin has potent inhibitory effects on endocrine pancreas and stomach but has no effect on exocrine pancreatic volume and enzyme secretion.
Pancreas 1988
PMID:Effects of somatostatin-14 on gastric and pancreatic responses to hormonal and neural stimulation using an isolated perfused rat stomach and pancreas preparation. 245 92

In streptozocin-induced diabetes in rats, there is a marked increase in the content and release of immunoreactive somatostatin (SLI) from the pancreas and upper gut. To elucidate whether these SLI changes are associated with alterations in somatostatin gene transcription, we measured somatostatin mRNA (SmRNA) accumulation in these and other SLI-producing tissues. Pancreas, stomach, jejunum, hypothalamus, and cerebral cortex were removed from control rats, 6-wk-diabetic rats, and diabetic rats treated with insulin for 6 wk. Total RNA was isolated by centrifugation through CsCl and fractionated on agarose gels. A sensitive radiodensitometric hybridization assay was used to determine SmRNA levels in absolute amounts by in vitro synthesized sense-strand RNA as a quantitative standard and antisense cRNA as a specific probe. SLI was determined by radioimmunoassay. SmRNA exhibited size heterogeneity between the different control and diabetic tissues. A 2- to 3-fold increase in total SmRNA was found in pancreas and stomach of the diabetic rats that suppressed toward normal with insulin treatment. These two tissues also exhibited significant 1.6- to 2.6-fold increases in SLI, respectively. The remaining tissues showed no diabetes-related changes in SLI or SmRNA. We conclude that in insulinopenic diabetes, tissue SLI and SmRNA accumulation undergo parallel changes; are increased in pancreas and upper gut, reflecting augmented somatostatin synthesis; are reciprocally related to insulin acting directly or indirectly on somatostatin-producing cells; and are unchanged in the lower gut and brain, suggesting tissue-specific regulation of somatostatin gene transcription in diabetes.
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PMID:Tissue-specific alterations in somatostatin mRNA accumulation in streptozocin-induced diabetes. 247 Jun 28

Developmental patterns for rat pancreatic opioid peptides and islet hormones were studied from gestational day 20 through adulthood. Fetal tissue was obtained as well as pancreas at birth (day 0), and postnatal days 3, 7, 14, and 21, and 7 weeks. The hormones measured included insulin, glucagon, and somatostatin. The opioids measured were beta-endorphin, Met- and Leu-enkephalins, and the high molecular weight enkephalin precursors. Pancreata were pooled as necessary and extracted (acid alcohol, or hot acetic acid), and opioids were further purified on reversed-phase C-18 (Sep-pak) cartridges. In all instances measurements were made by radioimmunoassays. Precursor peptides were first digested (with trypsin and carboxypeptidase B) prior to immunoassay. All opioids and hormones except the precursors for enkephalins showed a well-defined surge in pancreatic concentration during the first postnatal week. In contrast, the precursors had the highest concentration in the fetus, and by the seventh day of life had decreased by greater than 50%. This progressive decrease may represent maturation of the enkephalin convertase and trypsin-like enzymes in the islets. The opioid and hormonal surges that we have described are similar to the surge in islet concentration of thyroid-releasing hormone (TRH) previously described in neonatal rat islets. It is suggested that these postnatal alterations in opioid and hormone concentration relate to a specific function in the development of the endocrine pancreas.
Pancreas 1989
PMID:Developmental patterns for pancreatic opioids in the rat. 253 May 76

Rats injected with streptozotocin and nicotinamide developed grossly visible islet cell tumors of the pancreas. During i.v. glucose tolerance tests, two populations of tumor-bearing rats were identified: fast responders exhibited significantly lower plasma glucose and markedly elevated plasma immunoreactive insulin (IRI) levels relative to those of the controls. In slow responders, the plasma glucose level was significantly elevated up to 2 h after glucose injection, and the plasma IRI level was lower than that of the controls. During in vitro perfusions with glucose at 300 mg/dl (16.7 mM), tumor-bearing pancreata of fast responders released elevated levels of IRI and immunoreactive somatostatin (IRS); after tumor removal, glucose-stimulated release of these hormones returned to control levels. However, during similar perfusions of pancreata from slow responders, the IRI and IRS release did not decrease after tumor removal, suggesting that the nontumorous pancreatic islets rather than the gross tumors of the slow-responder group were the source of the glucose-stimulated hormone release. These studies demonstrate that gross tumors in the two responder subgroups differ in their glucose-stimulated hormone release.
Pancreas 1989
PMID:Glucose-stimulated hormone release in rats bearing streptozotocin/nicotinamide-induced islet adenomas: evidence for slow and fast responders. 254 77

In this study, liver metastases from a patient with a pancreatic glucagonoma producing the syndrome have been investigated histologically, ultrastructurally, and immunocytochemically. A comparison has also been made between the metastases and the primary pancreatic tumor investigated in a parallel study. In the metastatic tissue, glucagon-, pancreatic polypeptide (PP)-, and somatostatin-containing cells were found together with a majority of cells without any immunoreactivity. Glucagon-positive cells were much more numerous than PP- and somatostatin-immunoreactive cells. As in the primary tumor, double immunogold staining of ultrathin sections demonstrated the co-existence of glucagon and PP immunoreactivities in most of the granulated cells, but PP immunolabeling was often faint, so that it probably could not be revealed by the PAP method in light microscopical sections. Such a finding, together with the histological and ultrastructural features, is consistent with an ontogenic and phylogenetic primitiveness of the metastatic cell population.
Pancreas 1989
PMID:A malignant tumor of the pancreas producing glucagonoma syndrome: immunocytochemistry and ultrastructure of liver metastases and comparison with the primary tumor. 254 78

Previous studies in diabetic animal models have demonstrated altered pancreatic islet-cell populations. To further characterize the diabetic syndrome in our athymic nude mouse colony, we studied the population of endocrine cells in pancreatic islets of 4-week-old normoglycemic and 8-week-old hyperglycemic athymic nude (nu/nu) mice using immunohistochemistry, morphometry, and electron microscopy. In normoglycemic 4-week athymic nu/nu mice, the proportions of B (insulin-secreting) cells and A (glucagon-secreting) cells were similar to those in control Balb/c mice; however, the D (somatostatin-secreting) cells were significantly decreased in nu/nu mice. The populations of B and A cells appeared to be normal in hyperglycemic 8-week-old nu/nu mice while there was a significant increase in the proportion of D cells when compared with the proportion in Balb/c mice. Electron microscopic studies indicated that the appearance of B and A cells was similar in the 8-week-old hyperglycemic nu/nu and in controls; however, the D cells appeared to be enlarged and were finely packed with electron-dense secretory granules. Radioimmunoassays of the pancreatic content (micrograms/g fresh pancreas) of insulin, glucagon, and somatostatin in pancreata in 8-week-old normal Balb/c and hyperglycemic athymic nude mice were similar; however, the somatostatin content was significantly increased in the 8-week-old hyperglycemic nu/nu mice compared with age and sex-matched controls. These results demonstrate an altered D cell population and an increase in somatostatin levels in the pancreatic islets of the hyperglycemic athymic nude mouse animal model.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1989
PMID:Assessment of pancreatic islet-cell population in the hyperglycemic athymic nude mouse: immunohistochemical, ultrastructural, and hormonal studies. 256 96

Membrane receptors for [D-Trp6]-luteinizing hormone-releasing hormone [( D-Trp6]-LH-RH), somatostatin (SS-14), and epidermal growth factor (EGF) were investigated in experimental N-nitrosobis-(2-oxopropyl)-amine (BOP)-induced pancreatic cancers of hamsters and in specimens of normal human pancreas and human pancreatic cancer obtained from autopsies. Membrane receptors for [D-Trp6]-LH-RH were absent in the pancreas of normal hamsters, but appeared after the carcinoma was induced with BOP. Binding capacity of SS-14 receptors was lower in membranes of BOP-induced pancreatic cancers than in the normal pancreas. In the BOP-induced pancreatic cancers, the receptors were also characterized following in vivo treatment of hamsters with microcapsules of the agonist [D-Trp6]-LH-RH, somatostatin analog RC-160, and the combination of both peptides, which resulted in significant tumor inhibition. Therapy with [D-Trp6]-LH-RH and RC-160, alone or in combination, decreased the binding capacity of receptors for [D-Trp6]-LH-RH, but increased Bmax for SS-14. There were no significant changes in characteristics of the EGF receptor following these therapies. Membranes from human pancreatic cancers showed binding sites for [D-Trp6]-LH-RH, but no binding was detected in normal human pancreas. The presence of receptors for LH-RH in pancreatic tumors of hamster and humans raises the intriguing possibility that LH-RH could be involved in complex interactions that contribute to the appearance of pancreatic cancer. The binding capacity of receptors for SS-14 in human pancreatic cancer membranes was lower, while Bmax for EGF was higher, as compared to normal pancreas.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1989
PMID:Membrane receptors for peptides in experimental and human pancreatic cancers. 257 55


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