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 specificity of glucagon determinations with two pancreatic-type glucagon antisera has been determined by means of gel permeation chromatography before and after treatment of human plasma with acetone and ethanol. Acetone precipitates the interfering high molecular mass substances apparent in the void volume and cross-reacting precursor fragments, while pancreatic glucagon is extracted to slightly more than 50%. Hence, acetone treatment is suggested as a suitable means of obtaining specific glucagon results in single samples. Ethanol also precipitates the high molecular mass substances, but partly extracts the precursor fragments in addition to the glucagon. Ethanol treatment is therefore suggested for chemical diagnosis of the glucagonoma syndrome in which the tumor often produces precursor fragments.
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PMID:Increased specificity of plasma glucagon radioimmunoassay by use of acetone extraction. 682 9

Ethanol suppressed, in a dose-related manner, glucose-induced insulin (IRI) release and thus delayed the disappearance of glucose from the blood of rats. Pretreatment with pyrazole, an alcohol dehydrogenase inhibitor, exacerbated the effect of ethanol on IRI release, glucose tolerance and glucagon (IRG) release. These results suggest that ethanol produces glucose intolerance by inhibiting glucose-induced IRI release and by augmenting IRG release. Moreover, these findings indicate that ethanol does not have to be metabolized completely in order to produce these effects.
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PMID:Acute pretreatment with pyrazole and ethanol: effects on glucose-induced changes in insulin and glucagon. 699 53

Plasma glucose, insulin (IRI) and glucagon (IRG) levels were determined in fasting unanesthetized rabbits following pretreatment of either saline or ethanol (1.5 g/kg p.o.) and i.v. infusion of either saline or arginine (10 mg/kg/min for 30 min). Ethanol lowered plasma glucose and IRI levels but raised IRG levels in rabbits infused with saline. Arginine-induced hyperglycemia and hyperinsulinemia were markedly suppressed by ethanol so that any further increase expected by the infusion of arginine was minimized. Thus, ethanol not only alters basal levels of IRI, IRG and glucose but also suppresses arginine-stimulated levels as well.
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PMID:Effect of ethanol on basal and arginine-stimulated plasma levels of glucose, insulin and glucagon in fasted unanesthetized rabbits. 700 81

The effects of varying concentrations of ethanol (1, 10, and 30 mM) and its metabolites (1 mM acetate and 1 and 10 mM acetaldehyde) on insulin and glucagon secretion induced by glucose (11.1 mM) and arginine (20 mM) were studied in isolated perfused pancreas of Sprague-Dawley rats. Ethanol and its metabolites did not significantly modify basal secretion of the two hormones. Ethanol reduced glucose-induced insulin secretion by means of a dose-related effect. Arginine-induced insulin output did not seem to be influenced to any significant degree. Acetate and acetaldehyde significantly inhibited glucose and arginine-induced insulin secretion. While ethanol (10 and 30 mM ) did not modify glucagon output during arginine perfusion, acetate and acetaldehyde markedly enhanced it. The block of insulin secretion and the increased secretion of glucagon could explain the diabetogenic effect of ethanol demonstrated in vivo. The mechanism by which ethanol acts on the pancreatic beta- and alpha-cells is discussed.
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PMID:Effect of ethanol, acetaldehyde, and acetate on insulin and glucagon secretion in the perfused rat pancreas. 702 Dec 70

Ethanol oxidation by hepatocytes from fasted rats was determined in the presence and absence of 0.2 mM ethyl hydrazinoacetate, a transaminase inhibitor which blocks the malate-aspartate cycle. 20 muM phenazine methosulfate caused the largest increase (nearly 150%) in ethanol utilization. 5 muM norepinephrine caused a 50% increase in ethanol oxidation, and most of this increase was caused by stimulation of the alpha-glycerophosphate shuttle, since it remained in the presence of ethyl hydrazinoacetate. 1 muM glucagon caused a 25% increase in ethanol uptake, and most of this increase was abolished by ethyl hydrazinoacetate, indicating that the malate-aspartate cycle was involved. 25 muM dinitrophenol increased ethanol use by 20% and this increase was nearly unaffected by ethyl hydrazinoacetate. The results indicate that ethanol utilization, under the conditions used, is primarily controlled by the capacity of the shuttle systems, and not by the capacity of the respiratory chain.
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PMID:Control of ethanol utilization by rat hepatocytes. 726 Jan 20

Are alcohol and glucose blood levels modified in fasting subjects taking ranitidine? This experience tries to simulate normal life conditions. Nine men, volunteer, aged from 24 to 29 years old, without any digestive symptoms, ate a standard lunch after five hours of fasting, took 0.35 g of alcohol per kg. Ethanol blood levels, glycemia and blood levels of insulin and glucagon were taken at regular intervals every 10 to 15 minutes during all the experiment (120 minutes). After the initial experiment, all subjects took 150 mg of ranitidine p.o. b.i.d. during seven days. Afterward they were submitted to the same protocol. Between both experiments no differences were found on blood levels of ethanol. Peak concentration, decreasing rate, and biodisponibility (estimated by area under the curve) did not change. There was a tendency to have a faster decrease in glucose blood level (p < 0.05). This study does not show any significant modification of ethanol metabolism after taking ranitidine p.o.; those results are differing from data already found with studies using cimetidine.
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PMID:[Effect of ranitidine on blood alcohol and glucose levels after ingestion of alcohol]. 787 16

We studied the effect of ethanol and calcium antagonism (nifedipine) on insulin- (n = 8) and glucagon-like peptide-1 (GLP-1) (n = 6) secretion in healthy subjects. Four experiments in random order were performed (control, ethanol, nifedipine, and combination). Intravenous glucose tolerance tests were performed with and without pretreatment with oral ethanol and nifedipine. Ethanol pretreatment was followed by increased insulin (ethanol vs. control; p < 0.01) and C-peptide (ethanol vs. control; p < 0.05) areas after intravenous glucose (0-20 min), indicating that ethanol augments insulin secretion. Calcium antagonism with nifedipine abolished the ethanol augmentation of insulin secretion (insulin area 0-20 min, ethanol vs. combination, p < 0.05; and C-peptide area 0-20 min, ethanol vs. combination, p < 0.01). The GLP-1 response (area 0-90 min) was not significantly affected by ethanol.
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PMID:The ethanol augmentation of glucose-induced insulin secretion is abolished by calcium antagonism with nifedipine: no evidence for a role of glucagon-like peptide-1 (GLP-1). 943 65

Ethanol has profound acute effects on hepatic metabolism. While many of these effects are mediated via the redox imbalance that accompanies hepatic ethanol oxidation via the alcohol dehydrogenase (ADH) pathway, there is increasing evidence that ethanol also perturbs hepatic metabolism via its modulation of cyclic AMP-mediated signalling pathways. This paper examines the effects of ethanol on glucagon-stimulated protein phosphorylation using SDS-PAGE to analyse the 32P-labelling of cytosolic peptides in isolated rat hepatocytes pre-equilibrated with 32PO4(3-). We show that ethanol has biphasic effects on glucagon-stimulated protein phosphorylation. At a low concentration (50 mM), ethanol decreased the phosphorylation of certain peptides, whereas at higher concentrations (100-200 mM) it increased the 32P-labelling of all of the eleven glucagon-stimulated cytosolic peptides. The non-metabolizable alcohol 2-methylpyrazole-2-ol had no effects on glucagon-stimulated protein phosphorylation. The ADH inhibitor 4-methylpyrazole at 150 mM ethanol concentration abolished the potentiating effect of ethanol on the glucagon-stimulated phosphorylation of most peptides. In conclusion, the results indicate that ethanol alters glucagon-receptor-dependent protein phosphorylation in isolated hepatocytes via a complex mechanism that is partially dependent on ethanol oxidation via ADH.
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PMID:Effects of ethanol on glucagon-stimulated protein phosphorylation in isolated hepatocytes. 1464 35

The "J shape" curve linking the risk of poor bone health to alcohol intake is now well recognized from epidemiological studies. Ethanol and nonethanol components of alcoholic beverages could influence bone remodeling. However, in the absence of a solid underlying mechanism, the positive association between moderate alcoholic intake and BMD remains questionable because of confounding associated social factors. The objective of this work was to characterize the short-term effects of moderate alcohol consumption on circulating bone markers, especially those involved in bone resorption. Two sequential blood-sampling studies were undertaken in fasted healthy volunteers (age, 20-47 yr) over a 6-h period using beer of different alcohol levels (<0.05-4.6%), solutions of ethanol or orthosilicic acid (two major components of beer), and water +/- calcium chloride (positive and negative controls, respectively). Study 1 (24 subjects) assessed the effects of the different solutions, whereas study 2 (26 subjects) focused on ethanol/beer dose. Using all data in a "mixed effect model," we identified the contributions of the individual components of beer, namely ethanol, energy, low-dose calcium, and high-dose orthosilicic acid, on acute bone resorption. Markers of bone formation were unchanged throughout the study for all solutions investigated. In contrast, the bone resorption marker, serum carboxy terminal telopeptide of type I collagen (CTX), was significantly reduced after ingestion of a 0.6 liters of ethanol solution (>2% ethanol; p <or= 0.01, RM-ANOVA), 0.6 liters of beer (<0.05-4.6% ethanol; p < 0.02), or a solution of calcium (180 mg calcium; p < 0.001), but only after calcium ingestion was the reduction in CTX preceded by a significant fall in serum PTH (p < 0.001). Orthosilicic acid had no acute effect. Similar reductions in CTX, from baseline, were measured in urine after ingestion of the test solutions; however, the biological variability in urine CTX was greater compared with serum CTX. Modeling indicated that the major, acute suppressive effects of moderate beer ingestion (0.6 liters) on CTX were caused by energy intake in the early phase (approximately 0-3 h) and a "nonenergy" ethanol component in the later phase (approximately 3 to >6 h). The early effect on bone resorption is well described after the intake of energy, mediated by glucagon-like peptide-2, but the late effect of moderate alcohol ingestion is novel, seems to be ethanol specific, and is mediated in a non-calcitonin- and a non-PTH-dependent fashion, thus providing a mechanism for the positive association between moderate alcohol ingestion and BMD.
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PMID:Moderate ingestion of alcohol is associated with acute ethanol-induced suppression of circulating CTX in a PTH-independent fashion. 1925 29

In the 1990s, the introduction of visceral transplantation fuelled interest in other innovative therapeutic modalities for gut rehabilitation. Ethanol lock and omega-3 lipid formulations were introduced to reduce the risks associated with total parenteral nutrition (TPN). Autologous surgical reconstruction and bowel lengthening have been increasingly utilized for patients with complex abdominal pathology and short-bowel syndrome. Glucagon-like peptide 2 analogue, along with growth hormone, are available to enhance gut adaptation and achieve nutritional autonomy. Intestinal transplantation continues to be limited to a rescue therapy for patients with TPN failure. Nonetheless, survival outcomes have substantially improved with advances in surgical techniques, immunosuppressive strategies and postoperative management. Furthermore, both nutritional autonomy and quality of life can be restored for more than two decades in most survivors, with social support and inclusion of the liver being favourable predictors of long-term outcome. One of the current challenges is the discovery of biomarkers to diagnose early rejection and further improve liver-free allograft survival. Currently, chronic rejection with persistence of preformed and development of de novo donor-specific antibodies is a major barrier to long-term graft function; this issue might be overcome with innovative immunological and tolerogenic strategies. This Review discusses advances in the field of gut rehabilitation, including intestinal transplantation, and highlights future challenges. With the growing interest in individualized medicine and the value of health care, a novel management algorithm is proposed to optimize patient care through an integrated multidisciplinary team approach.
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PMID:The concept of gut rehabilitation and the future of visceral transplantation. 2560 64


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