Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of neurotensin on insulin and somatostatin release were examined in isolated pancreatic islets prepared from 3-4 days rats, and maintained in culture for 48 h before use. In the presence of 12 mM glucose, glucagon (50-2,000 ng/ml, i.e. 14-560 nM) caused a 2-fold increase in insulin and somatostatin release. Neurotensin (150 ng/ml, i.e., 100 nM) did not affect the glucagon-stimulated release, nor did it alter the release of either peptide measured at 12 mM glucose in the absence of glucagon. In contrast, neurotension markedly inhibited the release of both insulin and somatostatin that was induced by 23 mM glucose. These observations suggest that neurotensin may modulate the release of insulin and somatostatin evoked by high glucose concentrations, but not that resulting from the action of glucagon on pancreatic islets.
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PMID:Neurotensin inhibits glucose but not glucagon-induced insulin and somatostatin release in isolated islets. 4 73

In the dog ileum, neurotensin cells stained with immunofluorescence or immunoperoxidase proved distinct from argentaffin (EC) cells, glucagon immunoreactive (GLI) cells and pancreatic peptide immunoreactive (PP) cells. Neurotensin cells showed various degrees of reactivity with Grimelius' silver. With electron microscopy, besides EC cells, large granule cells with a thin peripheral rim of Grimelius-reactivity (L cells) and large granule cells with variable Grimelius-reactivity of the core (N cells) were found. On distributive grounds, L cells were identified with GLI cells and N cells were interpreted as neurotensin cells.
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PMID:Histochemical and ultrastructural identification of neurotensin cells in the dog ileum. 7 47

Isolated pancreatic islets were used to determine whether substances of hypothalamic origin could directly influence the release of insulin and glucagon. Media in which various regions of the brain had been incubated were tested in the islet system, as were the synthetic peptides neurotensin and substance P, and the catecholamines, dopamine and norepinephrine. Substance(s) released from the ventromedial hypothalamic (VMH) segments in vitro inhibited insulin release and stimulated glucagon release from the islets. Incubates of ventrolateral hypothalamic (VLH) or cortex tissue failed to alter insulin or glucagon levels. The VMH medium retained these activities even after oxidation with K3Fe (CN)6, whereas the ability of the catecholamines to inhibit insulin release and stimulate glucagon release was eliminated by this treatment. Neurotensin and substance P (0.1 and 1.0 nmol/ml) inhibited insulin release while glucagon release was increased; however, radioimmunoassay indicated that these peptides were virtually absent from the VMH incubate. These results show that incubates of VMH contain substances which can inhibit insulin and stimulate glucagon release in vitro. They may influence the endocrine pancreas by way of the peripheral circulation although the possibility of their occurrence in or near the pancreas itself has not been excluded.
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PMID:Effects of hypothalamic factors on insulin and glucagon release from the islets of Langerhans. 32 54

The effects of neurotensin on the release of insulin, glucagon, and somatostatin were investigated in isolated pancreatic islets prepared from 3- to 4-day-old rats and maintained in culture for 48 h before use. Islets were incubated for 20 and 60 min in the presence of 3 or 23 mM glucose with or without neurotensin. In 20-min incubations at 3 mM glucose, neurotensin (10-100 nM) increased the release of insulin, glucagon, and somatostatin by 60%, 90%, and 110%, respectively. These increases were not detected in 60-min incubations. Neurotensin (100 nM) inhibited the release of both insulin (by 60-90%) and somatostatin (by 100%) which was induced by 23 mM glucose in 60-min incubations; this inhibitory effect could be detected with neurotensin at a concentration of 1 nM. Neurotensin also significantly inhibited the elevations in glucagon, insulin, and somatostatin release induced by 20 mM arginine. It is concluded that neurotensin exerts a dual effect on the endocrine pancreas in vitro: 1) at low glucose concentration and over short term (20 min) incubations, the peptide stimulates insulin, glucagon, and somatostatin release; and 2) under stimulated conditions (high glucose or arginine), neurotensin inhibits insulin, glucagon, and somatostatin release.
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PMID:Effect of neurotensin on insulin, glucagon, and somatostatin release from isolated pancreatic islets. 37 97

It has been reported that Xenopsin, Neurotensin and Substance P change plasma glucagon and insulin levels when they are administered in vivo. In order to clarify whether these agents have a direct effect on glucagon and insulin secretion from the pancreas, the action of each substance was examined by using the rat pancreas perfusion technique. The results were as follows: The perfusion with 1 and 5 nmole/min of Xenopsin for ten minutes resulted in a significant but transient release within two minutes. Neurotensin did not show any stimulatory effect on glucagon release in the concentration of 1 or 5 nmole/min for ten minutes. However, Substance P lowered significantly the glucagon concentration in the perfusate in a similar concentration. None of these substances influenced significantly insulin release from the perfused pancreas. These findings suggest that the hyperglucagonemia caused by these three agents in vivo may not be attributed to the direct effect on the pancreatic A-cell.
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PMID:[Glucagon-releasing activity of xenopsin, neurotensin and substance P in the perfused rat pancreas (author's transl)]. 63 79

Neurotensin and substance P given iv 5, 10, 20 and 30 minutes prior to blood collection produce hypoinsulinemia, hyperglucagonemia and hyperglycemia in the rat. Glucagon similarly produces hyperglycemia in rats but results in hyperinsulinemia. On a molar basis neurotensin is ca. 10 and 30 times more active in inducing hyperglycemia than substance P and glucagon, respectively. The enhanced glucogenic effects of neurotensin and substance P over glucagon may well result from their inhibition of insulin release. Neurotensin and substance P may be important in glucose homeostasis.
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PMID:Effects of neurotensin and substance P on plasma insulin, glucagon and glucose levels. 126 3

The regional distribution and relative frequency of argyrophil cells, and of cells immunoreactive for 5-hydroxytryptamine (5-HT), substance P (SP), somatostatin, glicentin, glucagon, bovine pancreatic polypeptide (BPP), gastrin, leucine-enkephalin, gastric inhibitory polypeptide (GIP), cholecystokinin, secretin, motilin, and neurotensin were studied in 9 segments from the gastrointestinal tract of cows (greater than 1 year old) and calves (less than 3 months old). Argyrophil cells, 5-HT-immunoreactive cells, and somatostatin-immunoreactive cells were distributed throughout the gastrointestinal tract, whereas the other immunoreactive cells were more restricted in distribution. Most endocrine cells were more numerous in the calf than in the cow. This feature was most conspicuous in the abomasum. In the abomasum, argyrophil cells in the cow and calf and 5-HT-immunoreactive cells in the calf were found predominantly in the fundic region, whereas somatostatin-immunoreactive cells and gastrin-immunoreactive cells in the cow and calf and 5-HT-immunoreactive cells in the cow were most numerous in the pyloric region. Substance P-, glucagon-, BPP-, and leucine-enkephalin-immunoreactive cells were rarely detected. In the small intestine, argyrophil cells, 5-HT-, SP-, somatostatin-, gastrin-, GIP-, cholecystokinin-, secretin-, and motilin-immunoreactive cells were most numerous in the duodenum. Neurotensin-, glicentin-, glucagon-, and BPP-immunoreactive cells were detected with the highest frequency in the ileum. In the large intestine, argyrophil cells and 5-HT-, glicentin-, BPP-, somatostatin-, glucagon-, and SP-immunoreactive cells occurred with the highest frequency in the rectum.
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PMID:Histologic and immunocytochemical study of endocrine cells in the gastrointestinal tract of the cow and calf. 241 Nov 74

Enteroendocrine cells immunoreactive for gastrin, bovine pancreatic polypeptide (BPP), glucagon (glicentin), 5-hydroxytryptamine (5-HT), somatostatin, secretin, motilin, gastric inhibitory peptide (GIP) and cholecystokinin (CCK) are scattered throughout the small intestinal epithelium of the newborn opossum and in all later postnatal stages examined. The number of BPP- and glucagon-immunoreactive cells is relatively high in the newborn and rapidly decreases until only occasional cells are present after the first postnatal week. Cells immunoreactive for GIP, CCK, 5-HT, motilin, gastrin and secretin increase in number with development. Secretin-, motilin-, CCK- and GIP-immunoreactive cells generally are concentrated proximally in the small intestine and as they increase in number, differentiate in more distal regions. The number of gastrin-immunoreactive cells actually decreases just prior to weaning but then increases at and after, weaning. Neurotensin-immunoreactive cells are unusual in that they do not appear until about the 74th postnatal day and then are first encountered in the distal small intestine. As development progresses they increase in number and appear in the more proximal regions. Cells immunoreactive for 5-HT at first increase but then decrease sharply at weaning only to increase markedly again after this time. In contrast, somatostatin-immunoreactive cells gradually decrease in number until weaning then dramatically increase. If the total number of enteroendocrine cells in the small intestine is considered, there is a gradual decrease from birth until weaning when a dramatic increase occurs. Cells immunoreactive for neurotensin, 5-HT and somatostatin are also found in the intestinal epithelium of the developing colon and caecum. Somatostatin- and 5-HT-immunoreactive cells are found throughout the colon in the newborn whereas neurotensin-immunoreactive cells, although observed initially in the proximal colon, do not form a significant population until weaning and then are concentrated distally.
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PMID:Enteroendocrine cells in the developing opossum small intestine and colon. 280 25

The ability of certain neuropeptides (glucagon, somatostatin, leu-enkephalin and neurotensin) to release known neurotransmitters (glycine, GABA, dopamine and 5-hydroxytryptamine) was tested in the chicken retina. Tritiated neurotransmitters were injected intravitreally in chicken eyes. After excision, the retina was stimulated in vitro with the neuropeptide in micromolar concentrations while monitoring the efflux of radioactivity from the retina. A rise of the efflux represents a stimulus dependent release. Neurotensin release [3H] glycine, [3H]dopamine and [3H]5-hydroxytryptamine. Leu-enkephalin released [3H]dopamine and somatostatin released [3H]5-hydroxytryptamine. Glucagon was without effect. [3H]GABA was not released by any of the neuropeptides.
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PMID:Neurotransmitter release by certain neuropeptides in the chicken retina. 286 56

Argyrophil cells were identified by the single-impregnation Grimelius technique in 11 of 28 (39%) Brenner tumors, accounting for less than 1% of the tumor cell population in all the cases. All tumors with argyrophil cells were stained to demonstrate calcitonin, somatostatin, gastrin, adrenocorticotropic hormone, neurotensin, insulin, glucagon, and serotonin; and four of them (three benign and one borderline) were also stained for chromogranins with the monoclonal antibody LK2H10. Serotonin was present in nine of the 11 cases with argyrophil cells. Neurotensin and somatostatin were found in one borderline tumor, which also contained serotonin. Chromogranin reactivity was demonstrated in all four cases in which it was examined. Ultrastructural examination of one tumor revealed that the argyrophil cells contained secretory granules, 80 nm in diameter, and had elongated cytoplasmic processes that extended between the more numerous nonargyrophil tumor cells. The argyrophil cells of Brenner tumors are similar to those of urothelium in the frequency with which they are immunoreactive for serotonin and the rarity with which they are reactive for peptide hormones. These cells differ from those of mucinous ovarian tumors, which often contain both serotonin and peptide hormones. The findings of this study lend additional support to the close similarity of the epithelial components of Brenner tumors and urothelium.
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PMID:Argyrophil cells in Brenner tumors: histochemical and immunohistochemical analysis. 353 Oct 49


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