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 distribution and the frequency of occurrence of nine types of gut endocrine cells were revealed using immunohistochemical methods in eight portions from the gastrointestinal tract of the chicken (Gallus gallus var domestica). In the proventriculus, somatostatin- and gastrin-releasing polypeptide (GRP)-immunoreactive cells were commonly found. Serotonin-, pancreatic glucagon-, and enteroglucagon-immunoreactive cells were uncommon. Avian pancreatic polypeptide (APP)-immunoreactive cells were rare. In the gizzard, numerous GRP-, and a small number of somatostatin-immunoreactive cells were observed. The pyloric region was characterized by the presence of abundant gastrin-, somatostatin-, and neurotensin-immunoreactive cells. Numerous serotonin-immunoreactive cells were detected in all portions of the intestine. Moderate numbers of neurotensin-immunoreactive cells were detected in all portions of the intestine except for the cecum. A few gastrin- and somatostatin-immunoreactive cells were detected in the duodenum and jejunum. A small number of pancreatic glucagon-immunoreactive cells were detected in the jejunum and ileum. Enteroglucagon-immunoreactive cells were detected in the small intestine in increasing numbers forwards the ileum. Motilin-immunoreactive cells were rare in the small intestine.
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PMID:An immunohistochemical study on the distribution of endocrine cells in the chicken gastrointestinal tract. 280 Jun 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

SMS 201 995 is a new long acting analogue of somatostatin. We have investigated its effect on basal and meal stimulated secretion of gut hormones and have shown that after a single s.c. injection of 50 micrograms it lowers significantly the basal plasma levels of pancreatic polypeptide, secretin, motilin, pancreatic glucagon and insulin, it also effectively suppresses the postprandial release of pancreatic polypeptide, gastrin, secretin, gastric inhibitory peptide, pancreatic glucagon and insulin. Except for the usual brief discomfort of an injection, no symptoms or untoward effects were observed.
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PMID:Effect of long acting somatostatin-analogue, SMS 201 995, on gut hormone secretion in normal subjects. 286 Nov 6

Barrett's epithelium refers to the presence of ectopic mucosal types in the squamous-lined oesophagus. Previous studies have documented argentaffin and argyrophil-positive cells as well as gastrin-like immunoreactivity in oesophageal tissue extracts from patients with Barrett's mucosa. In the present study, 125 oesophageal biopsies obtained under direct vision at endoscopy from 22 patients with Barrett's oesophagus were systematically studied using fluorescence and peroxidase antiperoxidase single and double-staining immunocytochemical methods employing highly specific antibodies to localize the following peptide-containing cell types in Barrett's mucosa: gastrin, somatostatin, gastric inhibitory polypeptide, motilin, neurotensin and pancreatic glucagon. In addition, EC cells were localized using a cytochemical silver staining method. The results of this study indicate that EC cells and gastrin- and somatostatin-containing endocrine cells are detectable in Barrett's epithelium.
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PMID:Regulatory peptides in Barrett's oesophagus. 286 40

Four monoclonal antibodies specific for somatostatin have been produced and characterized. These antibodies were used to assess the anatomical relationship of somatostatin-containing cells in the pancreas and gastrointestinal tract of man, baboon and rat with ten other peptide-containing endocrine cells. The peptides investigated were gastrin, cholecystokinin, motilin, secretin, neurotensin, gastric inhibitory polypeptide, gut-glucagon, pancreatic glucagon, pancreatic polypeptide and insulin. The only regions in which somatostatin cells were seen in close contact with another endocrine cell were in the pancreas and the gastric antrum. In the pancreas somatostatin cells were commonly seen in close contact with insulin, glucagon and pancreatic polypeptide cells and infrequent contact was demonstrable with the gastrin-immunoreactive cells in the antrum of both rat and man. In all other cases no evidence was obtained for a close anatomical relationship between somatostatin cells and the other enteroendocrine cells.
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PMID:An immunocytochemical investigation with monoclonal antibodies to somatostatin. 286 26

We measured multiple components of serum or plasma in 221 members of a kindred with familial multiple endocrine neoplasia type 1 (FMEN1). The kindred showed typical features of FMEN1; the FMEN1 gene could be traced through 7 generations with 74 members identifiable as gene carriers. Between family screening in 1981 and completion of our study in 1985, we identified 16 previously unscreened members as carriers of the FMEN1 gene. The earliest age at diagnosis of FMEN1 was 17. The tests with the greatest yield of abnormal results among carriers of the FMEN1 gene were albumin-adjusted calcium, PTH, gastrin, and (in females) prolactin. The following tests provided little or no use in identifying carriers: prolactin (in males), pancreatic polypeptide, glucagon, glicentin, insulin, growth hormone, motilin, and somatostatin. Primary hyperparathyroidism was the commonest expression of the FMEN1 gene; the gene penetrance for this trait increased from near 0% before age 15 to near 100% after age 40. It appeared prior to development of serious morbidity from hypergastrinemia or hyperprolactinemia. All 42 co-operating members who were alive and expressing the FMEN1 gene in 1984 showed active or treated primary hyperparathyroidism. Primary hypergastrinemia had a prevalence below half of that for primary hyperparathyroidism at all ages and was not diagnosed in the absence of primary hyperparathyroidism. Primary hyperprolactinemia was still less prevalent than primary hypergastrinemia. It was limited almost exclusively to females.
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PMID:Multiple endocrine neoplasia type I: assessment of laboratory tests to screen for the gene in a large kindred. 287 98

SMS 201-995 (5-100 micrograms) injected subcutaneously in normal and type-2 diabetic subjects 30 min before a test meal caused dose-related suppression of plasma concentrations of insulin, glucagon, and several regulatory gut peptide hormones (gastrin, gastric inhibitory peptide, pancreatic polypeptide, secretin, neurotensin, and motilin). Effective hormone suppression was achieved even at the lowest dose of 5 micrograms. In the normal subjects SMS caused postprandial hyperglycaemia, but there was no overall deterioration in glucose tolerance in the type-2 diabetic patients. This suggests that counterregulatory hormones play an important part in the metabolic disturbance of type-2 diabetes.
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PMID:Postprandial effects of SMS 201-995 on gut hormones and glucose tolerance. 287 9

SMS 201-995 is an octapeptide analogue of somatostatin. The effect of a single subcutaneous (s.c.) injection of 50 micrograms SMS 201-995 on post-prandial intermediary metabolism was investigated in normal subjects. In spite of a long-lasting post-prandial suppression of insulin secretion, there were no significant changes in the plasma concentration of alanine, glycerol, 3-OH-butyrate or lactate. However, SMS 201-995 impairs carbohydrate tolerance, probably due to inhibition of insulin secretion. Basal and post-prandial plasma concentrations of the gut regulatory peptides pancreatic glucagon, motilin, pancreatic polypeptide, gastric inhibitory polypeptide, enteroglucagon, gastrin and peptide YY were suppressed up to 5 hours after subcutaneous administration of a single dose of SMS 201-995.
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PMID:The effect of a long-acting somatostatin analogue (SMS 201-995) on intermediary metabolism and gut hormones after a test meal in normal subjects. 297 76

This study examined the effects of transmural nerve stimulation, acetylcholine, adrenoceptor agonists and several peptides on the contractility of strips of human gallbladder in vitro. Acetylcholine caused concentration-related contractions of the tissues and the sensitivity to acetylcholine was similar in gallbladders with mild and severe chronic cholecystitis. Noradrenaline and adrenaline relaxed gallbladder strips, probably via beta 2-adrenoceptor stimulation. Transmural nerve stimulation always caused contractions, but in the presence of atropine inhibitory responses were demonstrable and these were antagonized by propranolol. There was no evidence of non-adrenergic inhibitory neural responses. Of the peptides tested, only cholecystokinin octapeptide (CCK-OP), gastrin, pentagastrin, substance P and caerulein caused contractions. Responses to CCK-OP, gastrin and pentagastrin were antagonized by dibutyryl cyclic GMP. Hormones which had no effect upon human gallbladder strips included motilin, secretin, bombesin, neurotensin, glucagon, vasopressin, VIP and somatostatin. Considerable differences therefore exist between human tissues and those from experimental animals with respect to the direct actions of neural and hormonal stimuli on gallbladder contractility.
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PMID:Contractility of human gallbladder muscle in vitro. 297 88

Within the past year, three similar peptides with specific growth hormone (GH) releasing effects have been extracted from human tissue, identified, and synthesized. Human pancreatic tumor GH releasing factor (I-40)-OH (hpGRF-40) was the sole hpGRF isolated from the pancreatic tumor of a patient in Charlottesville and was the predominant peptide isolated from the pancreatic tumor of a patient in Lyon. The Lyon tumor also contained hpGRF(1-37)-OH and hpGRF(1-44)-NH2. Both immunological and biochemical data suggest that hpGRF-40 and hpGRF-44 are present in the human hypothalamus and may be the human GH releasing hormone(s) (GHRH). In cultures of rat pituitary cells, hpGRF stimulates GH but affects neither basal and dopamine-inhibited prolactin release nor basal and gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) release. hpGRF stimulates cyclic AMP production within seconds, an effect which is blocked by somatostatin. In contrast, while hpGRF stimulates phosphatidylinositol turnover in the pituitary, the effect is not inhibited by somatostatin. In the human, hpGRF-40 (1 microgram/kg) given intravenously (i.v.) stimulates GH release within 5 minutes. hpGRF-40 does not elevate serum prolactin levels, thyrotropin (TSH), LH, or corticotropin (measured indirectly through plasma cortisol), or blood glucose or plasma concentrations of insulin, glucagon, pancreatic polypeptide, cholecystokinin, gastrin, gastric inhibitory peptide, motilin, or somatostatin. When graded doses of hpGRF (0.1-10 micrograms/kg) are given i.v., no differences are noted in the maximal levels of serum GH achieved.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human pancreatic tumor GH-releasing factor. 298 23


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