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)

Pancreas and gut hormones are involved in many endocrine and gastrointestinal diseases. Radioimmunoassays for these hormones have proved particularly valuable in diagnosis, localisation and control of treatment of endocrine tumours, of which many are mixed. An estimate based on ten years experience in a homogenous population of 5 million inhabitants (Denmark) suggests, that endocrine gut tumour-syndromes on an average appear with an incidence of 1 patient per year/syndrome/million. At present six different syndromes are known: 1) The insulinoma syndrome, 2) The Zollinger-Ellison syndrome.3) The Verner-Morrison syndrome. 4) The glucagonoma syndrome. 5) The somatostatinoma syndrome, and 6) the carcinoid syndrome. Accordingly diagnostically valuable RIAs for pancreas and gut hormones include those for insulin, gastrin, VIP, HPP, glucagon, somatostatin, and presumably also substance P. It is probably safe to predict that the need for gut and pancreas hormone RIAs within the next decade will increase greatly in order to assure proper management of tumours producing gastroentero-pancreatic hormones.
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PMID:Radioimmunoassay in diagnosis, localization and treatment of endocrine tumours in gut and pancreas. 22 84

To determine if pancreatic glucoregulatory hormones can be implicated in the glucose fall of pregnancy, we have measured plasma immunoreactive insulin and glucagon (IRI and IRG) in rats. Fed rats in midgestation show a rise in IRI without a corresponding increase in IRG. In late gestation, IRG rises significantly, but only enough to keep pace with a further rise in IRI. On a molar basis, IRI remains the predominant hormone despite a marked fall in blood glucose. After a 48-h fast IRI falls to comparably low levels in pregnant and virgin rats. A small rise in IRG is seen in virgin but not in pregnant rats despite frank hypoglycemia in the latter. Thus, IRG secretion in pregnancy is diminished relative to IRI in the fed state and fails to increase in the fasted state despite the stimulus of a lower glucose in both instances. To evaluate IRG secretory reserve, the IRG response to i.v. alanine was assessed in late gestation. In fed rats a greater IRG increase is seen in pregnancy; after fasting no difference is seen between pregnant and virgin rats. These results preclude an absolute deficiency in glucagon secretion. Pancreas hormone stores were alos measured in an effort to explain the altered secretory state. We find reciprocal changes in IRI and IRG content favoring IRG in midgestation and IRI in late gestation. Thus, pancreas hormone storage is altered in pregnancy but does not account for the changes in hormone secretion. Rather, pregnancy exerts an effect on the islet secretory process itself. Release of IRI is enhanced relative to IRG regardless of the blood sugar level. These observations suggest that in the pregnant rat circulating levels of insulin and glucagon may act to limit hepatic glucose output. Available evidence from the literature supports the concept of restrained glucose production. It is proposed that a lower blood glucose production. It is proposed that a lower blood glucose in rat pregnancy may be a lesser liability teleologically than would be the obligate nitrogen wasting which accompanies gluconeogenesis.
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PMID:Plasma glucagon and insulin in rat pregnancy. Roles in glucose homeostasis. 110 77

The cellular sequence of intraislet vascular perfusion has been shown to be important in the regulation of islet hormone secretion in the rat and dog islet. In order to test whether a B to A to D sequence of islet cellular perfusion is also present in a nonhuman primate, pancreata from the rhesus monkey, Macaca mulatta, were isolated and perfused in vitro in the presence and absence of anti-insulin gamma globulin. In the presence of the insulin antibody, efflux concentration of insulin decreased rapidly (-95 +/- 1.8%), whereas glucagon and somatostatin concentrations increased (111 +/- 28% and 239 +/- 38%, respectively). These results suggest the presence of a B-A-D cellular sequence of vascular perfusion within the monkey islet. The present results also strongly support the hypothesis that a B-A-D sequence of islet perfusion is important in the regulation of islet hormone secretion and further emphasize the central role of the B-cell in intraislet cellular interactions. The results also suggest that, despite differences in islet anatomy, a B-A-D order of islet cellular perfusion may be the preferred functional sequence among mammalian species.
Pancreas 1992
PMID:Perfusion with anti-insulin gamma globulin indicates a B to A to D cellular perfusion sequence in the pancreas of the rhesus monkey, Macaca mulatta. 137 78

The present study was designed to examine the contribution of the postprandial increase of plasma amino acids after ingestion of a protein-rich meal to the rise of the three pancreatic hormones insulin, glucagon, and pancreatic polypeptide (PP). A mixed amino acid solution was designed, which permitted a fairly close imitation of the arterial plasma pattern of the 21 amino acids that rise after ingestion of a 200-g porcine steak meal. In 10 healthy subjects the intravenous infusion of this mixed amino acid solution at a rate of 10 g/h elicited a rise of the 21 amino acids examined that correlated well with the postprandial increase (r = 0.89, p < 0.001). The maximal rise of plasma insulin (64 +/- 5 pmol/L) and glucagon (630 +/- 21 ng/L) was not significantly different from the postprandial increase of these two hormones (49 +/- 4 pmol/L and 780 +/- 28 ng/L, respectively). PP levels rose by 316 +/- 33 ng/L postprandially, which was clearly above the increase of 112 +/- 13 ng/L during intravenous amino acids (p < 0.01). In conclusion, the present data demonstrate that the postprandial rise of amino acid levels in arterialized venous plasma can account for most if not all of the postprandial increase of insulin and glucagon during the ingestion of a protein-rich meal. In contrast, only 35% of postprandial PP levels can be ascribed to the rise of plasma amino acids. In contrast to the effect of carbohydrate-rich meals, an enteric augmentation of insulin release seems to be of minor and possibly of no importance during ingestion of protein-rich meals.
Pancreas 1992
PMID:Contribution of postprandial amino acid levels to stimulation of insulin, glucagon, and pancreatic polypeptide in humans. 144 57

Pancreas transplantation, when successful, is the only reproducibly effective method to normalize glycemia without the use of exogenous insulin treatment in patients with diabetes mellitus. Worldwide success rates for combined pancreas and kidney transplantation are approximately 70%, and patient survival rates are approximately 90% one year postoperatively, although certain institutions have higher rates. Benefits of this procedure include normalization of fasting plasma glucose, hemoglobin A1C, glucose-induced insulin secretion, and intravenous glucose tolerance. Improvements are observed in glucose recovery following insulin-induced insulin hypoglycemia, glucagon secretion during hypoglycemia, kidney structure, and both motor and sensory nerve function. However, no benefits are accrued in pancreatic polypeptide secretion, kidney function, and the retinal pathology of diabetes mellitus. Further progress in these therapeutic results must await improvements in drugs for induction of immunosuppression, methods to induce immune tolerance, or provision of the operative procedure to patients less compromised preoperatively with secondary complications of diabetes.
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PMID:Pancreas transplantation as therapy for diabetes mellitus. 158 May 98

This study evaluated the in vivo effects of endotoxin and interleukin-1 (IL-1) on the simultaneous secretion of glucagon and insulin. The hypothesis that endotoxin, or IL-1 as a mediator, induces hyperglucagonemia secondary to pancreatic hypersecretion of glucagon was examined. Hormone secretion was measured using the in vitro perfused rat pancreas preparation. In response to an arginine stimulus, glucagon secretion was neither stimulated nor inhibited significantly by endotoxin or IL-1. Insulin secretion was significantly potentiated with both endotoxin and IL-1. In response to a low-glucose stimulus, glucagon secretion was significantly inhibited by endotoxin treatment, while insulin secretion was increased by endotoxin or IL-1. These results indicate that neither endotoxin nor IL-1 treatment resulted in glucagon hypersecretion, although either of these agents could induce insulin hypersecretion. Thus, the mechanism of endotoxin-induced hyperglucagonemia cannot be explained by a hypersecretory state of glucagon secretion. The parallel respective effects of endotoxin and IL-1 on glucagon and insulin secretion are consistent with the concept that IL-1 mediates some of the effects of endotoxin on the endocrine pancreas.
Pancreas 1992
PMID:Effects of endotoxin and interleukin-1 on glucagon and insulin secretion from the perfused rat pancreas. 159 58

Using sixteen cases (sixteen lesions) of endocrine tumor of the pancreas, found in 1,300 consecutive autopsy cases (661 men and 639 women; mean age, 79.0 years), we examined distribution patterns of pancreastatin (PST) in these endocrine tumors and in normal tissues around them, using immunohistochemical staining. In addition, the distribution patterns of PST was compared with those of insulin (INS), glucagon (GLU), somatostatin (SOM), and pancreatic polypeptide (PP), in these tissues. Normal islets of Langerhans were stained completely and evenly for PST. Two endocrine tumors did not stain for PST at all, six were partially stained, and eight were stained as densely as normal islets, or even more densely. Acinar cells were only partially stained for PST in 11 cases and showed scattered staining in three cases. Epithelial cells of ducts or ductuli were partially stained for PST in 10 cases and showed scattered staining in three cases. Distribution patterns of PST coincided with that of INS in 56% (9/16) of cases, GLU in 81% (13/16), SOM in 31% (5/16), and PP in 31% (5/16). In the eight tumors that were stained at least as densely for PST as normal islets, the staining pattern did not coincide with that of INS in any case (0%), coincided with that of GLU in all 8 cases (100%), and coincided with those of SOM and PP in one case each (13%). Therefore, the distribution of GLU-producing cells (A cells) coincided most closely with that of PST. It is concluded that most PST is secreted from A cells in human pancreas.
Pancreas 1991 Nov
PMID:Immunohistochemical study of the distribution of pancreastatin in endocrine tumors of the pancreas and in normal pancreatic tissue: analysis of autopsy cases. 168 79

We attempted to examine the immunopathological change of the pancreatic islets of newly diagnosed Type 1 (insulin-dependent) diabetic patients and thereby to obtain useful information for the therapy of the patients. For this purpose, pancreas biopsy under laparoscopy was performed 2-4 months after the onset of Type 1 diabetes in seven newly diagnosed patients. All biopsies were performed safely without any complications. Immunohistochemical examination of the biopsy specimens revealed a marked decrease of insulin-containing cells, preservation of glucagon-containing cells, and various degrees of expression of MHC class I and class II antigens in islet cells and in endothelial cells within and around the islets. Signs of active autoimmune phenomena, e.g. lymphocytic infiltration or immunoglobulin deposition in islets, were not detected in any of these patients by light microscopical evaluation. We conclude that pancreas biopsy under laparoscopy has shown various immunological changes in the islets of newly diagnosed Type 1 diabetic patients. Pancreas biopsy, however, may not be suitable under the present protocol for the selection of patients for immunotherapy because of problems including sampling errors.
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PMID:Examination of islets in the pancreas biopsy specimens from newly diagnosed type 1 (insulin-dependent) diabetic patients. 169 24

The synergistic impact of glucagon-like peptide-1 (GLP-1) (7-36)amide and cholecystokinin-8 (CCK-8) was studied in the rat pancreas. The GLP-1 (7-36)amide (1 pM-1 microM) had no effect on the basal or CCK-stimulated (1 nM-1 pM) amylase release from isolated pancreatic acini. The insulinotropic action of 0.5 nM GLP-1 (7-36)amide, which weakly stimulated the glucose-induced (6.7 mM) insulin release from the isolated perfused rat pancreas, was strongly potentiated by the addition of CCK-8 (20, 50, and 100 pM) to the perfusate. In concentrations as they occur physiologically after a meal, CCK-8 alone had no significant effect on basal or glucose-stimulated (6.7 mM) insulin secretion. Our data support the assumption that the nutrient-regulated intestinal release of various peptides represents a regulatory system to ensure an adequate insulin response to food intake, at least in rats.
Pancreas 1990 May
PMID:Interaction of glucagon-like peptide-1 (7-36)amide and cholecystokinin-8 in the endocrine and exocrine rat pancreas. 169 1

A spontaneously developed endocrine-exocrine pancreatic dysfunction was observed in the aged males of an inbred strain of Wistar rats, WBN/Kob. Nonobese male WBN/Kob rats developed glycosuria and hyperglycemia at around 9 months of age. Cumulative incidence of diabetes in male rats was 43% (33 of 76) at 12 months of age and reached 90% at the age of 21 months. In contrast, female rats did not become diabetic. Urinary excretion of amylase in WBN/Kob rats was significantly increased in comparison with control Wistar rats. Moreover, the exocrine pancreatic function test was impaired in WBN/Kob rats. Pathological examination of pancreata revealed infiltration of inflammatory cells, hemorrhage, deposition of hemosiderin, and fibrinous exudation around pancreatic ducts and blood vessels at 3 months of age. A gradual increase of fibrous tissue into the exocrine tissue and islets was observed with advancing age. The extremely enlarged interlobular lymph nodes were also observed. At the age of 12 months, the fibrous tissue replaced extensive areas of the pancreas and involved islets. The amylase content of pancreata in WBN/Kob rats was markedly decreased in comparison with that in Wistar rats at 12 months of age. Islets composed of few endocrine cells were detected. Immunohistochemical staining for insulin and glucagon showed a decreased number of not only B cells but also A cells. Moreover, both the pancreatic insulin and glucagon contents were markedly decreased in WBN/Kob rats in comparison with Wistar rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Pancreas 1990 Jul
PMID:Diabetic strain (WBN/Kob) of rat characterized by endocrine-exocrine pancreatic impairment due to distinct fibrosis. 169 84


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