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 study was prompted by the apparent detection of insulin antibodies in a black patient with HCC and recurrent hypoglycemia who had never received insulin. It consisted of two parts. Initially the sera of 30 individuals (six normoglycemic HCC patients, three with HCC and recurrent hypoglycemia, 11 patients with noncancerous liver diseases, and 10 healthy black controls) were analyzed for the presence of insulin (and glucagon) antibodies by precipitating the bound, labeled hormone with ethanol and also by the technique of radioimmunoelectrophoresis. In the nine HCC patients, binding of 125I-insulin averaged 13% by ethanol separation and 0.018 mU/ml with radioimmunoelectrophoresis, levels that were similar to those of patients with noncancerous liver disease and significantly higher than those of the healthy controls. Mean binding of 125I-glucagon was 11% in HCC sera. Serum binding of labeled hormones correlated significantly with IgG concentrations in the patients. The second part of the study attempted to define the nature of insulin binding in HCC and other forms of liver disease. After confirmation of the increased serum binding of labeled insulin by another method of precipitation, PEG, an attempt was made to compete with the labeled insulin for its serum binding sites by adding a large amount of unlabeled insulin. This binding was not displaceable, however, and was therefore considered nonspecific. When the same procedures were repeated using normal serum to which increasing amounts of gamma globulin were added, the nonspecific binding of insulin increased in a linear fashion. Furthermore, a similar degree of high nonspecific insulin binding occurred in six patients with multiple myeloma and raised serum IgG concentrations. We therefore conclude that in the many clinical situations where hypergammaglobulinemia exists, false positive tests for the detection of antibodies against insulin (and probably other peptide hormones) will emerge unless appropriate methods are used to check for nonspecific peptide binding.
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PMID:Nonspecific blinding of insulin to gamma globulin in the serum of black patients with hepatocellular carcinoma and other forms of liver disease. 618 Jan 12

Plasma amino acid, plasma pancreatic glucagon and serum insulin levels were simultaneously measured in cirrhotic patients with (drinkers) and without a history of alcohol drinking (non-drinkers), as compared to those in alcoholics without liver disease. Clinical characteristics in drinkers and non-drinkers, such as the extent of liver dysfunction, which may affect plasma amino acid levels, were strictly matched. Plasma pancreatic glucagon levels in the drinker group were much higher than those in the non-drinker group. In the former group, the elevated plasma pancreatic glucagon levels were correlated (p less than 0.05) to total amino acid levels (the sum of 20 kinds of L-amino acid concentrations) and, elevated AAA concentrations leading to a diminished BCAA/AAA ratio. Drinkers with histories of hepatic encephalopathy presented grossly elevated glucagon levels and severely abnormal aminograms similar to those observed in hepatic insufficiency.
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PMID:Characteristic features of plasma amino acid, plasma pancreatic glucagon, serum insulin concentrations in cirrhotic patients with histories of chronic alcohol consumption. 637 63

In the present investigation, insulin sensitivity and fasting levels of insulin, C-peptide, glucagon, growth hormone and free fatty acids were estimated and correlated in a population of individuals suffering from liver cirrhosis or chronic hepatitis. Insulin sensitivity, assessed by glucose disappearance rate after intravenous bolus injection of insulin, was reduced but not significantly different from controls in subjects with chronic persistent hepatitis, while it was significantly reduced in individuals suffering from chronic active hepatitis or liver cirrhosis. Insulin, glucagon, growth hormone, and free fatty acid fasting levels were higher than in healthy subjects in individuals with liver cirrhosis or chronic active hepatitis but not in subjects with chronic persistent hepatitis. C-peptide concentrations did not differ from controls in subjects with liver disease. Significant negative correlations occurred between coefficients of insulin sensitivity and fasting concentrations of insulin, glucagon, growth hormone and free fatty acids, but not with fasting levels of C-peptide. Positive relationships were present between fasting levels of free fatty acids and both glucagon and growth hormone concentrations. These results show that, unlike subjects with liver cirrhosis and chronic active hepatitis, individuals suffering from chronic persistent hepatitis do not differ from healthy subjects in insulin sensitivity and fasting levels of insulin, glucagon, growth hormone, and free fatty acids. Moreover, they suggest that both hyperinsulinemia and high concentrations of counterregulatory substances might play a role in the pathogenesis of insulin resistance in subjects suffering from chronic liver disease.
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PMID:Possible roles of insulin, glucagon, growth hormone and free fatty acids in the pathogenesis of insulin resistance of subjects with chronic liver diseases. 639 73

The effects of insulin and glucagon administration on serum amino acid levels were investigated in patients with severe liver disease, since simultaneous injection of pancreatic hormones has been recently introduced as a therapeutic approach. The changes in serum amino acid concentrations, as observed 3 h after ceasing a 3 h infusion of insulin and glucagon in 500 ml glucose solution, were an elevation of serum branched chain amino acid (BACA) levels and of the molar ratio of BCAA/aromatic amino acid (AAA) levels in patients with liver cirrhosis. Similar increases of serum BCAA levels during the infusion were also observed in patients with fulminant hepatitis. The results suggest that insulin-glucagon therapy for severe liver disease has no harmful side effects at least with respect to alterations in the serum aminogram.
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PMID:Effects of insulin and glucagon on serum amino acid concentrations in liver disease. 676 Jun 74

A randomized, double-blind, controlled trial of insulin and glucagon infusion was conducted in 50 patients with acute alcoholic hepatitis. Twenty-five treatment patients received 24 U regular insulin and 2.4 mg glucagon over 12 h daily for 3 wk. Twenty-five control patients received 200 ml dextrose solution in identical bottles over the same time period. Six control and 2 treatment patients died from liver failure during study, and another treatment patient died from hypoglycemia. In the 34 patients with prothrombin times greater than 3 s prolonged, fewer deaths occurred among the insulin- and glucagon-infused patients (p less than 0.10). Clinical features of liver disease on entry into the study were similar in the two groups, and total serum bilirubin and prothrombin time improved more rapidly in the treatment group (p less than 0.05). Insulin and glucagon infusion is a promising treatment of alcoholic hepatitis and merits further study in the most severely ill patients.
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PMID:A randomized clinical trial of insulin and glucagon infusion for treatment of alcoholic hepatitis: progress report in 50 patients. 701 49

The contribution of hyperammonemia to plasma amino acid imbalance in patients with liver disease was assessed in 10 subjects with chronic hepatitis and in 17 advanced cirrhotics. Insulin, glucagon, and plasma amino acids were determined both in the basal state and 45 min after oral ammonium chloride, at doses used in the ammonia-tolerance test. In cirrhotics, ammonia increased to 3 times basal values, in association with a rise in insulin and, more marked, in glucagon. Aromatic amino acids and free tryptophan further increased, while a significant fall in branched-chain amino acids and glutamate was observed. The increase in ammonia levels strongly correlated with the increase in glucagon (r = 0.707). Two patients, with large esophageal varices, showed signs of disturbed consciousness, in association with a marked rise in ammonia and in the ration of free tryptophan to the sum of neutral amino acids. In patients with chronic hepatitis, whose ammonia levels rose slightly, minor variations in pancreatic glucoregulatory hormones and plasma amino acids were observed, as also happened in 10 healthy subjects following ammonium chloride ingestion. Our data fit with the hypothesis that the plasma amino acid imbalance of cirrhotics may be partly due to ammonia-induced changes in pancreatic hormones.
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PMID:Ammonia-induced changes in pancreatic hormones and plasma amino acids in patients with liver cirrhosis. 704 53

Pancreatic glucagon (IRG) levels in the postabsorptive (fasting) state and in response to arginine test (ATT), have been investigated in 17 subjects with porto-caval anastomosis (PCA). Out of these, seven subjects were insulin-treated diabetics, 5 were untreated diabetics, and 5 had no evidence of clinical diabetes. Basal and stimulated IRG values in the overall group of PCA subjects were significantly increased in comparison to 14 normal controls. No significant difference was found between the three groups of patients in respect to IRG values. The mean fasting IRG levels, grouped in relation to the age of shunt, were significantly raised six months after surgery. In addition no significant difference in IRG values (fasting or stimulated) was observed in relation to the entity of the liver disease (child degree) or to the type of surgical shunt. Finally, when PCA patients with or without encephalopathy were considered, fasting and peak IRG values were significantly increased in those patients with encephalopathy.
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PMID:Exaggerated glucagon secretion in diabetic and non-diabetic subjects with surgical porto-caval anastomosis. 729 9

Acute alcoholic hepatitis is the first alcoholic lesion of the liver in the process of progression to cirrhosis. It is due to the toxic action of alcohol on hepatocytes, in particular in the centrolobular region. It may affect a liver which is the site of fatty infiltration, fibrosis or cirrhosis, i.e. during all the stages of alcoholic liver disease. Its severity depends upon the degree of alcoholic intoxication. It may be fatal by malignant hepatic failure in a quarter of cases or, at the extreme, be totally asymptomatic. The aims of treatment are: 1) in the immediate, to prevent death; 2) subsequently, to prevent progression to cirrhosis. The majority of the wide range of treatments suggested have been evaluated in controlled trials. It is thus easy to show that corticosteroids are effective in severe acute alcoholic hepatitis, i.e. with encephalopathy and coagulation disturbances, but no in ordinary forms. Although logical, nutritional supplements, whether enteral or parenteral, have no influence on the course of acute alcoholic hepatitis. The same applies to anabolic steroids, the association insulin-glucagon, antifibrosis agents or "hepatoprotectors". The elimination of alcoholic intoxication remains the most important point, accepted by all hepatologists.
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PMID:[Treatment of acute alcoholic alcoholism]. 768 Jan 91

The objective of this study was to determine the relations between the hallmark circulatory finding of decompensated cirrhosis, a reduced systemic vascular resistance (SVR), and the indices of hepatic decompensation, the accumulation of ascites, and the concentrations of various vasoactive substances. At a university-affiliated teaching hospital, eighteen hospitalized patients with cirrhosis and 18 age- and sex-matched healthy subjects were used. This was a case-control study. Measurements included cardiac dimensions and indices derived from echocardiograms and Doppler studies, abdominal ultrasound estimates of ascites, indices of hepatic function, and various serum (S) and urinary (U) substances. Results showed that cirrhotics had increased left atrial and left ventricular dimensions, left ventricular mass, heart rate, cardiac output (CO), transvalvular velocities, and a decreased SVR. SVR was related to hepatic dysfunction, as reflected by an abnormal prothrombin time ratio (r = -0.64, p = 0.006), and also related to overall severity of liver disease as estimated by the Child-Pugh score (r = -0.53, p = 0.044). Although cirrhotics with ascites generally had a reduced SVR, estimates of ascites were directly related to SVR (r = 0.57, p = 0.03) and inversely related to CO (r = -0.53, p = 0.04). Concentrations of S and U digoxin-like immunoreactive substance (DLIS) were also increased, but the concentrations of S glucagon and estradiol were not elevated. The accumulations of S and U DLIS, S glucagon, and S estradiol were all related to hepatic dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasodilatory state of decompensated cirrhosis: relation to hepatic dysfunction, ascites, and vasoactive substances. 777 37

In man and experimental animals, portal hypertension with portal-venous collaterals, is associated with a hyperdynamic circulation, caused by peripheral vasodilatation, mainly in the splanchnic bed. This peripheral vasodilatation is clinically important, since it is thought to be responsible for the pathogenesis of complications of portal hypertension such as ascites, the hepatorenal syndrome and portal hypertensive gastropathy and colopathy. Many cirrhotic patients may not die primarily because of their hepatic dysfunction, but rather because of the consequences of the circulatory abnormalities which are secondary to the liver disease. Circulating hormonal vasodilators from intestinal origin such as glucagon, insufficiently cleared by the liver, are only partly responsible for these changes. Recent experimental data point to a role for an increased production of the locally acting potent vasodilator nitric oxide in the vascular wall, in the pathogenesis of the hyperdynamic circulation. Furthermore, nitric oxide seems to play an important role in the development of portal-venous collaterals. Modulation of the nitric oxide production might offer therapeutic options for the treatment of portal hypertension and its complications.
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PMID:Haemodynamic changes in portal hypertension: new insights in the pathogenesis and clinical implications. 805 7


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