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 need for chaotropic eluents in immunoaffinity chromatography is a consequence of the high affinities of antibodies towards their antigens. This affinity is decreased and elution of antiglucagon antibodies from a column of immobilized glucagon can be achieved under mild conditions when the steric complementarity to the antibody binding site is perturbed by selective chemical modification of the hormone. The effects of reaction with 2-hydroxy-5-nitrobenzyl bromide, tetranitromethane and hydrogen peroxide have been studied. Conversely, treatment of immobilized antibodies with 2-hydroxy-5-nitrobenzyl bromide facilitates the elution of glucagon during immunoaffinity chromatography. The general implications of these results are discussed.
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PMID:Avoidance of strongly chaotropic eluents for immunoaffinity chromatography by chemical modification of immobilized ligand. 0 98

A method for tubeless, double-contrast examination of the small bowel is described. Oral contrast medium and capsules which effervesce in the small bowel resulted in double-contrast demonstration of the small bowel in 90 out of 130 patients. Transit through the small bowel was reduced to an average of 78 minutes, due to increased peristalsis resulting from distension by the intralumental gas. For comparison, average transit time in a control group of 83 patients was found to be 126 minutes. The differential diagnosis of stenosing processes and additional information concerning space-occupying lesions was furthered by small bowel hypotonia induced by the intravenous injection of 15 to 45 mg. propantheline bromide (Probanthine) or 1 to 2 mg. glucagon. The method has the following advantages: 1. Improved demonstration of detailed mucosal pattern, 2. Reduced examination time and 3. Simultaneous visualisation of the entire small bowel.
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PMID:[Double-contrast examination of the small bowel without intubation (author's transl)]. 13 39

Twelve patients with known esophageal varices and willingness to cooperate were included in the study. Medications administered were placebo, 2 mg of glucagon, and 30 mg of propantheline bromide. All medications were given double-blind and crossover. On the basis of this study the authors believe that for optimal visualization of esophageal varices the following is the procedure of choice: (1) the patient should remain horizontal (this is best done in the left lateral position for comfort and ease of expectoration) for ten minutes after swallowing high density barium; (2) the patient should "clear his throat" frequently and expectorate all saliva (barium sticks to the pharynx and makes the patient want to swallow and "clearing his throat" by forced expiration helps the patient to expectorate this coating and prevents swallowing); (3) filming should be done in expiration in the supine (left posterior oblique to table top) position; and (4) in equivocal cases the examination can be repeated with an anticholinergic drug if the patient has no contraindications to its use. The patient should empty his bladder just before administration of the drug. The intelligent use of these factors should result in a saving of both fluoroscopic time and film, and give the radiologist a safe optimal diagnostic yield.
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PMID:Optimal visualization of esophageal varices. 17 97

Glucagon1-21 has been prepared by treating native glucagon with carboxypeptidase A. Purified glucagon1-21 did not contain detectable methionine (less than 0.001 residue/mol) and the activity of the compound did not change after treatment with cyanogen bromide as has been shown with native glucagon. Glucagon1-21 stimulates hepatic adenylate cyclase activity to the same extent as native glucagon but with 0.1% the potency. Glucagon1-21 also displayed 0.1% the binding affinity of native glucagon to the glucagon receptor in hepatic membranes. Glucagon22-29 alone or in combination with glucagon1-21 did not activate adenylate cyclase or displase 125I-glucagon from its receptor. The finding that glucagon1-21 is a full agonist on adenylate cyclase is discussed in relation to the structure-function relationships required for the biological action of glucagon.
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PMID:A reassessment of structure-function relationships in glucagon. Glucagon1-21 is a full agonist. 21 Jan 80

The hypotonic effect of glucagon (2 mg) and propantheline bromide (Pro-Banthine, 30 mg) on the upper gastrointestinal tract was compared in a double-blind study in 12 healthy volunteers and 36 patients. The solvent solution for the two drugs was used as a placebo. Both drugs and placebo were administered intramuscularly. The time of onset of the hypotonic effect was similar for both drugs, with maximum effect achieved 10 min after injection. Effects of glucagon dissapeared rapidly after 30 min, while Pro-Banthine still retained 50% of its maximum effect 2 1/2 hr after injection. Side effects of Pro-banthine were related to the long duration of the hypotonic effect (4-6 hr). A significant placebo effect on the duodenal C loop was observed. Glucagon appears to be the drug of choice since its hypotonic and hypomotile effects on the gastrointestinal tract are comparable to propantheline bromide while having the advantage of shorter duration and practically no side effects.
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PMID:Double-blind evaluation of glucagon and propantheline bromide (pro-banthine) for hypotonic duodenography. 40

The electrocardiogram was monitored in 100 patients undergoing oesphago-gastro-duodenoscopy. Premedication differed: 25 patients each were given either (Group I) atropine 0.5 mg, hyoscine-N-butylbromide 20 mg, and diazepam 5 mg, or (Group II) hyoscine-N-butyl-bromide 20 mg and diazepam 5 mg, or (Group II) diazepam 5 mg and glucagon 0.2 mg, or (Group IV) only diazepam 5 mg intravenously. After injection of the parasympatholytic drugs (Groups I and II) there was a significantly higher heart rate duringthe entire length of the examination than in groups III and IV. Nine of the ten cases of ascending S-T depression were found in Groups I and II, while descending (ischaemic) S-T changes occurred equally frequently in patients of all four groups. Two of the three more serious arrhythmias were registered after atropine. Since parasympatholytic drugs fail to inhibit arrhythmias and ST-T changes, while accentuating the rise in heart rate, it is recommended that premedication for oesophago-gastro-duodenoscopy should not include such drugs.
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PMID:[Cardiac side-effects of oesophago-gastro-duodenoscopy in relation to premedication (author's transl)]. 68 92

Various preparations of glucagon treated with chloramine-T under different conditions have been studied with respect to their immunoreactivity toward two different glucagon antisera; one specific for pancreatic glucagon and the other capable of reacting with enteroglucagon as well. The glucagon preparations exposed to chloramine-T for different periods reacted almost identically with the nonspecific antibody whether they were used as tracer or standard. On the contrary, treatment with chloramine-T under severe conditions led to reduced immunoreactivity toward the specific antibody. Inclusion of dimethyl sulfoxide (DMSO) in the chloramine-T reaction resulted in preservation of the immunoreactivity of the treated preparations. The cyanogen bromide cleaved-glucagon, (1-26) homoserine lactone, showed little cross-reactivity with the specific antibody whereas it reacted to a similar extent with the nonspecific antibody as natural glucagon did. Amino acid analysis of the hormone exposed to chloramine-T demonstrated that the methionine residue at position 27 in the glucagon molecule had been oxidized to methionine sulfoxide. In addition, tryptophan had also been affected. DMSO protected methionine and tryptophan from the oxidative action of chloramine-T. We postulate from these results that the change in the immunoreactivity toward the specific antibody of glucagon exposed to chloramine-T is mainly due to oxidation of the methionine residue at position 27 in the molecule. The usefulness of DMSO in the iodination process is also discussed.
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PMID:Effect of an exposure to chloramine-T on the immunoreactivity of glucagon. 116 32

Administration of dehydroepiandrosterone (DHEA) to rats results in alterations in liver and serum factors. This study was undertaken to determine the earliest metabolic change(s) associated with DHEA treatment. Serum cholesterol, triacylglycerol, glucose, insulin, glucagon, thyroid hormones and hepatic glucose-6-phosphate dehydrogenase activity were, in general, unaltered in obese Zucker rats after 7 d and 24, 12 and 3 h of DHEA treatment. Malic enzyme, long-chain fatty acyl-coenzyme A hydrolase and catalase activities and peroxisomal beta-oxidation rates were elevated after 7 d and 24 h in DHEA treatment, but not after 12 h. Mitochondrial beta-oxidation was not altered. Hepatic mitochondrial state 3 respiration per g liver with glutamate-malate was elevated after 7 d and 24, 12 and 3 h in DHEA-treated rats and was elevated per mg protein except after 7 d. Succinate-supported state 3 respiration per g liver was also elevated after 7 d and 24 and 12 h of DHEA treatment. Mitochondria from rats treated for 7 d had lower levels of cardiolipin and phosphatidylethanolamine and an increase in phosphatidylcholine. Changes in fatty acid composition of these phospholipids occurred after 7 d and 24 h of DHEA treatment. In an additional study, rats were treated with DHEA or DHEA plus ethidium bromide for 3 d. Ethidium bromide inhibited the increase in mitochondrial protein and respiration associated with DHEA treatment. These findings indicate that mitochondrial respiration is the earliest factor affected by DHEA and may be associated with protein synthesis.
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PMID:Short-term effects of dehydroepiandrosterone treatment in rats on mitochondrial respiration. 182 28

The presence of adenosine receptors coupled to adenylate cyclase in rat heart sarcolemma is demonstrated in these studies. Heart sarcolemma was isolated by the hypotonic shock-Lithium bromide treatment method. This preparation contained negligible amounts (2-4%) of contamination by other subcellular organelles such as mitochondria, sarcoplasmic reticulum, and myofibrils as verified by electron microscopic examination. In addition this preparation was also devoid of endothelial cells, since angiotensin-converting enzyme activity was not detected in this preparation. N-Ethylcarboxamide adenosine (NECA), L-N6-phenylisopropyladenosine (PIA), and adenosine N'-oxide (Ado N'-oxide) were all able to stimulate adenylate cyclase in heart sarcolemma, but not in crude homogenate, with an apparent Ka of 3-7 microM. The activation of adenylate cyclase by NECA was dependent on the concentrations of metal ions such as Mg2+ or Mn2+. The maximal stimulation was observed at lower concentrations of the metal ions (0.2-0.5 mM). At 5 mM Mg2+ or Mn2+, the stimulation by NECA was completely abolished. The stimulatory effect of NECA on adenylate cyclase was also dependent on guanine nucleotides and was blocked by 3-isobutyl-1-methylxanthine. In addition, 2'-deoxyadenosine showed an inhibitory effect on adenylate cyclase. The myocardial adenylate cyclase was also stimulated by beta-adrenergic agonists, dopamine and glucagon, and inhibited by cholinergic agonists such as carbachol and oxotremorine. The stimulation of adenylate cyclase by NECA was found to be additive with maximal stimulation obtained by epinephrine. These data suggest that rat heart sarcolemma contains adenosine (Ra), beta-adrenergic, dopaminergic, glucagon, and cholinergic receptors, and the stimulation of adenylate cyclase by epinephrine and adenosine occurs by distinctly different mechanism or adenosine and epinephrine stimulate different cyclase populations.
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PMID:Regulation of adenylate cyclase by adenosine and other agonists in rat myocardial sarcolemma. 241 61

Exposure of cultured hepatocytes to glucagon leads to a partial refractoriness of the adenylate cyclase both to glucagon (homologous desensitization) and to isoproterenol (heterologous desensitization). In contrast, isoproterenol produces a very strong homologous desensitization but almost no heterologous desensitization. The present study compared the pattern of the homologous and heterologous components of glucagon-induced desensitization in these cells, particularly during the first 4 hours, and examined the role of cyclic 3',5'-adenosine monophosphate (cAMP) in the mechanism of refractoriness development. The decrease in glucagon-sensitive and isoproterenol-sensitive adenylate cyclase activities were closely parallel with respect to the extent, the time course and the dose required. 8-Bromoadenosine 3',5'-monophosphate (8-Bromo-cAMP) also reduced the hormone-responsive adenylate cyclase activity, but this effect developed more slowly than the desensitization after glucagon treatment. No consistent relationship was found between cAMP levels and induction of hormone refractoriness when the cells were exposed to glucagon, isoproterenol, cholera toxin or forskolin. Furthermore, addition of 0.5 mM 3-isobutyl-1-methylxanthine) (IBMX) which strongly amplified the cAMP response, did not potentiate the glucagon-induced desensitization of either glucagon-sensitive or isoproterenol-sensitive adenylate cyclase activity. Taken together, the results suggest that homologous and heterologous desensitization of the adenylate cyclase developing after glucagon exposure occur by similar (agonist-non-specific) mechanisms which do not involve cAMP.
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PMID:Glucagon-induced refractoriness of hepatocyte adenylate cyclase: comparison of homologous and heterologous components and evidence against a role of cAMP. 247 64


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