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)

In the present study, following a double-blind, double placebo protocol vs. placebo, we compared the hypotonic effect of intranasal and intravenous glucagon during a double-contrast barium meal examination of the stomach. We found a statistically significant difference between placebo and intranasal or intravenous glucagon in inducing gastric hypomotility, with no significant differences between IN and IV glucagon. The intranasal administration of glucagon has the advantage of being noninvasive and well tolerated by the patients, and might be a valuable aid in upper gastrointestinal examination as well as in CT scan or magnetic resonance imaging of the abdomen.
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PMID:The hypotonic effect of intranasal and intravenous glucagon in gastrointestinal radiology. 789 98

Barium enema examinations establish the presence of neoplastic or inflammatory disease in the colon. Areas of narrowing commonly encountered appear to represent organic disease. These areas are in expected locations throughout the colon and have been described. Not much attention had been given to these areas in recent literature, however, which has led to unnecessary colonoscopies and even surgeries. The sphincters of Rossi, Balli, and Payr-Strauss are involved in nerve reflexes; the sphincters of Hirsch, Moultier, and Busi are a thickening of longitudinal and circular muscle fibers. Cannon's sphincter is an overlap of the superior and inferior mesenteric nerve plexuses. When an area of narrowing is encountered where a known sphincter is located, insufflation of more air, changing patient position, administering 2 mg of glucagon intramuscularly or 0.5 mg to 1 mg intravenously will aid in the distinction between a sphincter and organic disease.
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PMID:Colonic sphincters revisited: simulators of organic disease. 800 17

In 1958, Welin recommended the routine use of atropine before a barium enema to reduce mucus secretion and make the examination more comfortable. Currently, many radiologists believe that smooth-muscle spasmolysis is a useful adjunct during a barium enema and use such a spasmolytic agent. One survey found that spasmolytic agents were administered more frequently in 1987 than in 1976. The use of glucagon had increased 20% between 1976 and 1987. Among 34 foreign institutions responding to the survey, 37% used glucagon and 45% used scopolamine butylbromide (Buscopan). Nevertheless, it is still controversial whether spasmolytic agents play a significant role in the performance and interpretation of a barium enema. Some radiologists routinely use a spasmolytic agent; others do so only selectively.
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PMID:The use of antispasmodic drugs during barium enemas. 819 92

The aim of this study was to compare the effects of a genetically engineered glucagon (geG) and hyoscine N-butylbromide (HBB) on the quality of double-contrast barium meal (DCBM) study. Two hundred sixty-four patients scheduled for DCBM were randomized to receive intravenously geG 0.25 mg (geG-25), or geG 0.5 mg (geG-50), or HBB 20 mg as hypotonic agent. The evaluation concerned: duration of isolated visualization of the stomach (A); gastric mucosal coating (B); visualization of areae gastricae (C); quality of duodenal cap (D) and loop (E) study; delay, if any, of duodenal study (F). Global significant differences (P from 0.0183 to < 0.0001) were found for A, C, D, and F. GeG-50 allowed the longest isolated gastric visualization (P < 0.0001); geG-25 allowed more extensive visualization of areae gastricae than HBB (P = 0.0006); HBB allowed a better study of duodenal cap (P = 0.0052) and loop (P = 0.0190) than geG-25; geG-50 prolonged the examination time (P < 0.01). No adverse effect was observed with geG within 1 h after DCBM. In conclusion, geG can be safely used as a hypotonic agent in DCBM. When DCBM is focused on the stomach, 0.25 mg of geG is the optimal choice; if DCBM is focused on the duodenum, 0.5 mg of geG (with a prolonged examination time) or 20 mg of HBB (with a less effective study of the stomach) should be used.
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PMID:Compared effect of a genetically engineered glucagon and hyoscine N-butylbromide on double-contrast barium meal study. 951 May 82

Glucagon is commonly used during gastrointestinal examinations for the temporary inhibition of gastroduodenal movements. Three preparations of glucagon are now clinically available: those prepared by extraction from the pancreas (GL-P), by chemical synthesis (GL-S), and by genetic recombination (GL-G). The aim of this study was examine the mechanism of the inhibitory effect of glucagon on gastrointestinal motility and the cause of its side effects by comparing three glucagon preparations. In four conscious dogs, gastrointestinal contractions were monitored by means of chronically implanted force transducers. Each glucagon preparation (GL-P [15 microg/kg], GL-S [5, 15, 45 microg/kg], GL-G [15 microg/kg]), scopolamine butylbromide (0.4 mg/ kg), or saline was administered intravenously 20 min after the termination of spontaneous phase III contractions, and blood samples were taken at 5- to 10-min intervals. Barium was administered into the stomach 10 min after the infusion of each drug. The arrival of a barium meal in the stomach immediately stimulated gastrointestinal contractions, and the barium meal was expelled into the duodenum and jejunum from the stomach. Intravenous injection of 15 microg GL-S first stimulated duodenal contractions that propagated to the jejunum, followed by strong inhibition of the barium-induced gastrointestinal contractions. This inhibitory effect of glucagon and the activity of the glucagon-induced duodenal contractions were dose-related. The inhibitory effects of GL-G and GL-S were stronger than that of GL-P. Blood glucose and plasma insulin concentrations were raised after intravenous injection of each glucagon preparation, but there was no difference among the three preparations and no dose relationship. The inhibitory effects of glucagon depend on the material purity and dose, and the inhibitory mechanism was independent of any effect on carbohydrate metabolism. Glucagon administration caused phase III-like contractions in the duodenum and jejunum, which may be responsible for the side effects of glucagon.
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PMID:Mechanism of inhibitory effect of glucagon on gastrointestinal motility and cause of side effects of glucagon. 985 56

A previous study had shown an increased prevalence (83%) of diverticula among patients with autosomal dominant polycystic kidney disease (ADPKD) with end-stage renal disease (ESRD) compared with other ESRD patients without ADPKD (32%). Others have also suggested an increased risk for diverticular complications in renal transplant recipients with ADPKD. To determine whether there was an increased occurrence of diverticula among non-ESRD patients with ADPKD, we studied 55 patients with ADPKD who were not receiving renal replacement therapy compared with 12 unaffected family members (non-ADPKD) and 59 random patients who had undergone barium enemas (control [C]). No study patient had a history of diverticular disease. All patients underwent a double-contrast barium enema after administration of glucagon. The occurrence, number, location, and size of diverticula were noted. There was no significant difference among the three groups in regard to sex (men: ADPKD, 42% versus non-ADPKD, 42% versus C, 37%) or age (ADPKD, 49.3 +/- 0.7 versus non-ADPKD, 51.2 +/- 2.1 versus C, 49 +/- 1 years). There was no significant difference in the percentage of patients with diverticula (ADPKD, 47% versus non-ADPKD, 58% versus C, 59%), the percentage with only right-colon diverticula (ADPKD, 5% versus non-ADPKD, 17% versus C, 5%), the mean number of diverticula in patients with diverticulosis (ADPKD, 13.8 versus non-ADPKD, 7.9 versus C, 9.9 diverticula), or the size of the largest diverticula (ADPKD, 9.5 versus non-ADPKD, 10.4 versus C, 10.5 mm). There was no significant difference in these variables between the patients with ADPKD with a creatinine clearance greater than 70 mL/min/1.73 m(2) (n = 25) or less than 70 mL/min/1.73 m(2). This study does not show the greater prevalence of diverticular disease in non-ESRD patients with ADPKD compared with the general population. Thus, patients with ADPKD need not be considered at greater risk for diverticular disease than the general population.
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PMID:Evaluation of colonic diverticular disease in autosomal dominant polycystic kidney disease without end-stage renal disease. 1056 Nov 42

Development of endocrine cells in the endoderm involves Atonal and Achaete/Scute-related basic helix-loop-helix (bHLH) proteins. These proteins also serve as neuronal determination and differentiation factors, and are antagonized by the Notch pathway partly acting through Hairy and Enhancer-of-split (HES)-type proteins. Here we show that mice deficient in Hes1 (encoding Hes-1) display severe pancreatic hypoplasia caused by depletion of pancreatic epithelial precursors due to accelerated differentiation of post-mitotic endocrine cells expressing glucagon. Moreover, upregulation of several bHLH components is associated with precocious and excessive differentiation of multiple endocrine cell types in the developing stomach and gut, showing that Hes-1 operates as a general negative regulator of endodermal endocrine differentiation.
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PMID:Control of endodermal endocrine development by Hes-1. 1061 24

Neuroendocrine tumors overexpressing the proglucagon- derived peptides have been associated with severe constipation. The relationship between two of the intestinal proglucagon-derived peptides, glucagon-like peptide (GLP)-1 and -2, and delayed gastrointestinal transit, was characterized in a patient with a neuroendocrine proglucagon-derived peptide tumor. A 60-yr-old female presented with intractable constipation and intermittent vomiting. Gastric, oral-ileal and colonic transit times, and plasma hormone levels were determined before tumor resection. Expression of the proglucagon-derived peptides by the tumor was determined by immunohistochemistry, Northern blot analysis, HPLC, and RIA. Oral-cecal transit was more than 3 h, and a barium follow-through study showed dilated and thickened folds with most of the barium concentrated in the ileum at 24 h; residual barium was identified in the colon at 14 d post ingestion. Circulating levels of GLP-1 and -2 were 300- to 400-fold elevated compared with levels in normal human subjects. Normal bowel function was restored by tumor resection. Consistent with the elevated plasma hormone levels, the tumor was found to express the proglucagon gene, and immunoreactive GLP-1 and -2 were detected by both immunohistochemistry and RIA. Overexpression of glucagon-like peptide-1 and -2 is associated with markedly prolonged gastrointestinal transit in humans. These findings are consistent with a role for these peptides in the regulation of gastrointestinal motility.
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PMID:Prolonged gastrointestinal transit in a patient with a glucagon-like peptide (GLP)-1- and -2-producing neuroendocrine tumor. 1210 4

Fasting triggers a series of hormonal cues that promote energy balance by inducing glucose output and lipid breakdown in the liver. In response to pancreatic glucagon and adrenal cortisol, the cAMP-responsive transcription factor CREB activates gluconeogenic and fatty acid oxidation programmes by stimulating expression of the nuclear hormone receptor coactivator PGC-1 (refs 2-5). In parallel, fasting also suppresses lipid storage and synthesis (lipogenic) pathways, but the underlying mechanism is unknown. Here we show that mice deficient in CREB activity have a fatty liver phenotype and display elevated expression of the nuclear hormone receptor PPAR-gamma, a key regulator of lipogenic genes. CREB inhibits hepatic PPAR-gamma expression in the fasted state by stimulating the expression of the Hairy Enhancer of Split (HES-1) gene, a transcriptional repressor that is shown here to be a mediator of fasting lipid metabolism in vivo. The coordinate induction of PGC-1 and repression of PPAR-gamma by CREB during fasting provides a molecular rationale for the antagonism between insulin and counter-regulatory hormones, and indicates a potential role for CREB antagonists as therapeutic agents in enhancing insulin sensitivity in the liver.
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PMID:CREB controls hepatic lipid metabolism through nuclear hormone receptor PPAR-gamma. 1461 8

Glucagon-like peptide-2 (GLP-2) is a neuropeptide secreted from endocrine cells in the gut and neurons in the brain. GLP-2 stimulates intestinal crypt cell proliferation and mucosal blood flow while decreasing gastric emptying and gut motility. However, a GLP-2-mediated signaling network has not been fully established in primary cells. Since the GLP-2 receptor mRNA and protein were highly expressed in the mouse hippocampus, we further characterized that human (125)I-labeled GLP-2(1-33) specifically bound to cultured hippocampal neurons with K(d) = 0.48 nM, and GLP-2 acutely induced subcellular translocalization of the early gene c-Fos. Using the whole cell patch clamp, we recorded barium currents (I(Ba)) flowing through voltage-gated Ca(2+) channels (VGCC) in those neurons in the presence of GLP-2 with and without inhibitors. We showed that GLP-2 (20 nM) enhanced the whole cell I(Ba) mediated by L-type VGCC that was defined using an L-type Ca(2+) channel blocker (nifedipine, 10 microM). Moreover, GLP-2-potentiation of L-type VGCC was abolished in neurons pretreated with a PKA inhibitor (PKI(14-22), 1 microM). Finally, using a fluorescent nonmetabolized glucose analog (6-NBDG) tracing imaging, we showed that glucose was taken up directly by cultured neurons. GLP-2 increased 2-deoxy-d-[(3)H]glucose uptake that was dependent upon dosage, activation of PKA, and potentiation of L-type VGCC. We conclude that GLP-2 potentiates L-type VGCC activity through activating PKA signaling, partially stimulating glucose uptake by primary cultured hippocampal neurons. The potentiation of L-type VGCC may be physiologically relevant to GLP-2-induced neuroendocrine modulation of neurotransmitter release and hormone secretion.
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PMID:GLP-2 potentiates L-type Ca2+ channel activity associated with stimulated glucose uptake in hippocampal neurons. 1992 Feb 20


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