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)

Using immunohistochemical techniques we studied duodenal biopsies from 18 patients with coeliac disease and 24 patients with normal duodenal morphology. We had access to antisera against the following gastrointestinal peptides: cholecystokinin (CCK), gastric inhibitory peptide (GIP), gastrin-17, glucagon-enteroglucagon, motilin, neurotensin, pancreatic peptide (PP), secretin, somatostatin, substance P and vasoactive intestinal peptide (VIP). The somatostatin, GIP, CCK, and glucagon cells were increased in number in coeliac disease. The number of motilin cells was slightly increased, while secretin cells were reduced. Cells storing gastrin-17, substance P, or neurotensin were rare in all patients regardless of diagnosis. No PP immunoreactive cells were found and VIP was localised to neurons only. In biopsies from patients having a mucosa with ridging of villi the number of the various endocrine cell types did not differ from that in the control group.
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PMID:Duodenal endocrine cells in adult coeliac disease. 38 55

While a patient was being evaluated for melena, a glucagon-induced hypotonic examination of the small intestine demonstrated a small ulcerated mass in the jejunum. The tubeless hypotonic examination was performed after multiple gastrointestinal series, small intestinal series, barium enemas, and visceral arteriography--including celiac and superior mesenteric arteriograms--failed to identify a bleeding site. Surgical exploration revealed three ulcerated lymphomatous lesions in the jejunum. The lack of side effects, rapidity of onset, and shortness of duration of intravenous glucagon suggest that this type of hypotonic examination of the small intestine may prove useful as an adjunct to the small intestinal series.
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PMID:Glucagon-induced small intestinal hypotonia demonstrating bleeding lymphoma. 76 46

The purpose of the present study was to evaluate the effects of several gastrointestinal hormones on the gastric submucosal arterioles using an in vivo microscopy technique. Alteration in diameter of submucosal arterioles, 40 to 90 mu in diameter, in response to infusion of different agents into the celiac axis, was measured in the anesthetized cat. Pentagastrin, the octapeptide of cholecystokinin, natural secretin, and histamine produced arteriolar dilation. Only with histamine and the octapeptide of cholecystokinin did this occur with doses that might be considered physiological. Synthetic secretin had no vasodilator activity, suggesting the presence of a contaminating agent in natural secretin. Glucagon had no effect on the submucosal arterioles. In addition, the effect of glucagon on the smaller (10 to 30 mu) terminal and subterminal submucosal arterioles was studied in the rat by in vivo microscopy. Again no effect was observed with glucagon, but norepinephrine in small doses produced vasoconstriction.
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PMID:The effect of gastrointestinal hormones on the gastric microcirculation. 95 93

Humoral immune factors related to type 1 diabetes have been investigated in children with coeliac disease. Anti-insulin (IAAb), immunoglobulin (alpha IgAb), islet cell (ICA) and glucagon autoantibodies were examined in 15 children with coeliac disease at diagnosis (group 1), in 15 children with coeliac disease following a gluten-free diet (group 2) and in 30 control patients (groups 3 and 4). IAAb were present in 27% of group 1 and in 20% of group 2 patients and alpha IgAb were significantly increased in group 1 and 2 patients; two patients in group 2 were positive for ICA; none of the coeliac disease patients were positive for anti-glucagon antibodies. The levels of anti-gliadin antibodies in group 1 were positively correlated with those of alpha IgAb. Coeliac disease-related HLA antigens were not correlated with antibody presence. The presence of diabetes-related humoral immune factors in coeliac disease raises the question as to whether or not they are predictive of subclinical pancreatic damage or whether they are simply indicators of a more general autoimmune diathesis.
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PMID:Diabetes-related autoantibodies do appear in children with coeliac disease. 139 82

A 49-year-old woman suffered from recurrent episodes of necrolytic migratory erythema over the lower legs, lower abdomen, and buttocks for more than two years. Stomatitis, glossitis and vaginitis were the accompanying symptoms and signs during each episode. The result of skin biopsy revealed superficial necrosis in the upper half of the epidermis. Laboratory examinations revealed mild glucose intolerance and hypoaminoacidemia. Fasting plasma glucagon level measured by radioimmunoassay was 890 pg/mL. Oral glucose loading test showed a paradoxical increase in plasma glucagon level up to 1,500 pg/mL. Abdominal echo, computerized axial tomography, and celiac angiography demonstrated a hypervascular tumor, 4 cm in diameters, located at the pancreatic head. Glucagonoma syndrome was confirmed and diagnosed. The patient underwent surgical resection of the tumor mass. Necrolytic migratory erythema disappeared thereafter, and the plasma glucagon level declined to 120 pg/mL. Histologically, the tumor revealed an islet cell carcinoma composed of moderately uniform cells with a few mitosis, arranged in cords and nests. Abundant characteristic secretory granules of the pancreatic A cell were found within the tumor cells by electron microscopic examination.
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PMID:[Necrolytic migratory erythema as the first manifestation of glucagonoma]. 168 96

Although it is generally acknowledged that pancreatic islets are under powerful vagal control, specifics of vagal pathways and their central representation in the brain stem are unclear. To define this circuitry, we combined a protocol measuring electrical vagal stimulation-induced insulin and glucagon secretion with a retrograde tracer strategy that delineated the pool of spared motoneurons in the dorsal motor nucleus of the vagus (dmnX) following selective abdominal branch vagotomies. Three of the five branches mediated both insulin and glucagon release: posterior gastric (+198 and +117% increase from basal for insulin and glucagon, respectively), anterior gastric (+177 and +104%), and hepatic branch (+103 and +60%). In contrast, unreliable and nonsignificant hormonal responses were produced by stimulation of fibers projecting through either the posterior celiac (+12% insulin and +12% glucagon) or accessory celiac (+15% insulin and +31% glucagon) branches. Since hexamethonium almost completely blocked both insulin and glucagon responses to stimulation, the effects are not likely to have resulted from inadvertent antidromic excitation of vagal afferents. Cell bodies of stimulated motoneurons, which were responsible for insulin and glucagon secretion, were found to occupy the medial two-thirds of the right (projecting through the posterior gastric branch) and left (projecting through the anterior gastric and hepatic branches) dmnX. These medial, longitudinal dmnX columns and their associated abdominal vagal branches are likely to play the predominant role in vagal control of the endocrine pancreas.
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PMID:Localization of vagal preganglionics that stimulate insulin and glucagon secretion. 196 14

To define the vagal circuitry mediating the cephalic phase insulin response (CPIR), this reflex was measured in conscious, freely moving rats that had previously undergone selective abdominal vagotomies that spared different columnar subpopulations of dorsal motor nucleus of the vagus (dmnX) neurons. The CPIR was defined as an increase of plasma insulin from basal at 2 min after the start of ingestion. The CPIR measured in peripheral blood after chow ingestion was reliable and significant (P less than 0.05) in rats with all branches intact, +24.9 +/- 5.1 microU/ml (+130% increase from basal); rats with only the two gastric branches and the hepatic branch intact, +27.0 +/- 3.5 microU/ml (+153%); and rats with only the hepatic branch intact, +13.5 +/- 4.8 microU/ml (+188%). No significant response occurred in animals with only the two celiac branches intact, +1.8 +/- 1.8 microU/ml (+15%) or in those with none of the branches intact, +3.9 +/- 3.3 microU/ml (+21%). The CPIRs measured in portal vein blood were generally larger but showed the same pattern across groups. Plasma glucose measurements of portal vein blood indicated that with chow ingestion no significant absorption had occurred by 2 min, whereas with either milk or glucose intake absorption did occur. Subsequent bilateral electrical cervical vagal stimulation-induced insulin and glucagon responses in the same animals under anesthesia showed the same branch dependency. It is concluded that the CPIR is mediated by the two gastric and the hepatic branches but not the two celiac vagal branches. The perikarya of the preganglionics innervating the pancreatic B-cells are contained within a large pool occupying the two medial columns of the dmnX.
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PMID:Identification of vagal preganglionics that mediate cephalic phase insulin response. 217 54

We hypothesized the existence of vagal arginine sensors in the liver which modulate arginine-induced pancreatic hormone secretion. The present study was carried out to examine the efferent pathways and receptor mechanisms from arginine sensors using selective vagotomies and autonomic drugs on the secretion of insulin and glucagon after ip injection of L-arginine (1 g/kg BW) in rats in an unanesthetized and unrestrained state. Hepatic vagotomy (sectioning of the hepatic branch of the vagus nerve) enhanced both plasma insulin and glucagon concentrations after ip arginine more than those in sham-vagotomized (control) rats. The effect of hepatic vagotomy was blocked by adding celiac vagotomy (sectioning of the celiac branches of the vagus nerve) or by previous administration of atropine methyl nitrate (10 mg/kg BW), but not by phentolamine (1 mg/kg BW) or propranolol (2 mg/kg BW). Celiac vagotomy alone did not affect the plasma insulin concentration; however, it reduced the plasma glucagon concentration after ip arginine compared to that in sham-vagotomized rats. Administration of atropine alone did not affect plasma insulin or glucagon concentrations after ip arginine. These results suggest that celiac branches of the vagus nerve act as efferent pathways to the pancreas through a muscarinic receptor mechanism in the hepatic arginine sensor-mediated pancreatic neuroendocrine system. The physiological role of these hepatic sensors may be to prevent arginine-induced exaggerated pancreatic hormone secretion and maintain blood glucose homeostasis.
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PMID:Modulation of arginine-induced insulin and glucagon secretion by the hepatic vagus nerve in the rat: effects of celiac vagotomy and administration of atropine. 220 80

Simultaneous intraperitoneal injection of pancreatic glucagon (PG) and cholecystokinin (CCK) results in a functionally synergistic satiety effect in non-deprived sham feeding rats ("PG-CCK satiety"). That is, PG and CCK together inhibit feeding significantly more than the sum of their individual effects. Because the individual satiety effect of each peptide on normal feeding is dependent on the abdominal vagus nerve, we tested the vagal mediation of this synergistic effect of PG plus CCK. Vagotomies were verified anatomically and, in one experiment, histologically. Total abdominal vagotomy blocked PG-CCK satiety. Neither selective vagotomies of the hepatic, the gastric, the celiac, the gastric and celiac, nor the gastric and hepatic branches, however, affected PG-CCK satiety. This indicates that the vagal contribution to the synergistic satiety effect of PG plus CCK on sham feeding is redundant. Although some vagal fibers are necessary for PG-CCK satiety, no individual branch is required for the effect, and at least two branches, the hepatic and celiac, are each sufficient for mediating it.
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PMID:Redundant vagal mediation of the synergistic satiety effect of pancreatic glucagon and cholecystokinin in sham feeding rats. 234 51

Pharmacological, percutaneous celiac plexus blockade is often inefficient in the treatment of pain in chronic pancreatitis. Lack of efficiency could be due to incomplete denervation of the plexus; however, a method for measuring the completeness of celiac plexus blockade is not yet available. We have, therefore, monitored the physiological completeness of pharmacological percutaneous celiac blockade with 40 ml 25% ethanol by measuring the effect of posture on heart rate, blood pressure, hepato-splanchnic vascular resistance, and pancreatic hormone concentrations before and after celiac plexus block in 6 patients with chronic pancreatitis. Blood pressure decreased and heart rate increased after the block (P less than 0.025), whereas no significant change was found in hepato-splanchnic vascular resistance nor in the change of these parameters during transition from the supine to standing position. Pancreatic hormones (C-peptide, free insulin, glucagon, pancreatic polypeptide and somatostatin) did not change in response to standing, either before or after the block. The cardiovascular variables were normalized the day after the block, and all the patients were in their habitual state regarding pain after 1 week. In conclusion, pancreatic hormone concentrations in response to standing are not useful for monitoring celiac plexus block, whereas heart rate, blood pressure and hepato-splanchnic blood flow may yield useful information. From such measurements it was concluded that permanent denervation of the celiac plexus was not achieved in our patients after injection of 40 ml 25% ethanol.
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PMID:Monitoring of celiac plexus block in chronic pancreatitis. 213 12


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