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)

Plasma glucagon-like immunoreactivity (GLI) levels were increased in patients with liver cirrhosis. The levels were not significantly correlated with plasma glucagon immunoreactivity (GI) and serum insulin levels. None of the conventional liver function tests were correlated with the GLI levels, although plasma GI levels were high in cirrhotics with hyperammonemia. A significant correlation between plasma GLI and amino acid levels was not observed in these cases. The oral glucose tolerance test (OGTT) showed a significant decrease of plasma GI levels in cirrhotics but no change of plasma GLI concentrations: cirrhotic patients with diabetes mellitus or total gastrectomy showed marked increases of GLI levels. Glucagon (Glucagon Novo) injection at a dose of 10 micrograms/kg body weight to cirrhotic patients produced marked increases of both GI and GLI levels rapidly, though the mechanism of GLI elevation could not be clearly explained.
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PMID:Elevation of plasma glucagon-like immunoreactivity (GLI) in patients with liver cirrhosis. 347 62

Carbohydrate intolerance is frequently seen in patients with hepatic cirrhosis. To study the role of the counter regulatory hormones, glucagon, cortisol and growth hormone in this disease, these hormones were measured in 11 patients with hepatic cirrhosis and six controls during a 4-hour oral glucose tolerance test (OGTT) and in five normal and cirrhotic subjects during steady-state plasma insulin and glucose concentrations (SSPGI) achieved with the euglycemic clamp technique. Fasting plasma glucose was 103 +/- 4.3 mg/dl in cirrhotics and 88 +/- 3.3 mg/dl in controls (p less than 0.001). Immunoreactive insulin (IRI) was 24.3 microU/ml in cirrhotics and 12.7 +/- 2.2 microU/ml in controls (p less than 0.001); immunoreactive glucagon (IRG) was 263 +/- 30 pg/ml in cirrhotics and 122 +/- 17.5 pg/ml in controls (p less than 0.001); serum growth hormone (GH) was 4.4 +/- 0.9 ng/ml in cirrhotics and 0.5 +/- 0.1 ng/ml in controls (p less than 0.001). During OGTT, the 2-hour glucose concentration was 201 +/- 9.7 mg/dl in cirrhotic subjects and 147 +/- 10.0 mg/dl in controls (p less than 0.001). IRG levels were suppressed by 20% of basal values in patients with cirrhosis, while controls showed 10% suppression after an oral glucose load. At 60 minutes, the serum GH was 14.7 +/- 3.9 ng/ml in cirrhotics and 0.3 +/- 0.1 ng/ml in controls (p less than 0.001). The normal suppressive effect of hyperglycemia on GH secretion in controls was sharply contrasted by a paradoxical elevation of serum GH in the cirrhotic group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Elevated growth hormone levels and insulin resistance in patients with cirrhosis of the liver. 351 47

In order to evaluate the pathogenesis of the systemic hyperdynamic circulation in portal hypertension, serum concentration of eight kinds of hormones including glucagon (Glu), aldosterone (Ald), renin (Ren), and epinephrine (Adr), and the hemodynamic parameters were measured in a series of 30 patients, of whom 23 were patients with liver cirrhosis, 3 were with Banti's disease, 2 with chronic active hepatitis, and 2 with pre-cirrhotic change. The average cardiac index was 4.6l/min, m2, with normal PCWP of 6.7 mmHg. CI. and SVR. showed significant inverse correlation of r = -0.767 (p less than 0.01), however, PCWP and CI did not have any significant correlation. Average serum concentrations of Glu, Ald, and Ren were 160 pg/ml, 139 pg/ml, and 5.4 ng/ml, respectively, all of which were increased up to 2.5 times above the normal values. Adr, norepinephrine, cortisol, estrone and estradiol were within normal limits. Of the eight hormones being measured, only Glu had significant correlation with both liver function tests and the cardiac index (r = 0.479, p less than 0.05). Neither Ald nor Adr had significant correlation with hemodynamic parameters.
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PMID:[Systemic hyperdynamic circulation and serum hormone concentrations in portal hypertension]. 352 13

Coexistence of hyperinsulinemia and normal or impaired carbohydrate tolerance indicates insulin resistance which is frequently observed in patients with liver diseases such as liver cirrhosis, fatty liver, acute and chronic hepatitis and idiopathic haemochromatosis. Insulin resistance in liver diseases can be due to circulating insulin antagonists or a target tissue defect in insulin action, either due to changes in the state of the insulin receptor or due to a postreceptor defect, that means any abnormality in the insulin action sequence following the initial binding step. High insulin levels in liver diseases are caused by diminished degradation of insulin by the liver whereas hypersecretion only plays a minor role under basal conditions. High levels of glucagon, free fatty acids and growth hormone are well known in liver diseases but until now there is no evidence of the pathogenetic importance of these factors. Conflicting results on insulin binding, methodological criticism on binding data and the question whether or not diminished insulin binding on peripheral blood cells plays any physiological role make it unlikely that studies on insulin receptors of peripheral blood cells contribute to the revelation of insulin resistance in liver diseases. The clamp technique allows to quantify the sensitivity of the body to exogenous insulin. The results on liver cirrhosis in connection with studies on glucose metabolism show that under basal conditions insulin insensitivity is due to peripheral resistance (primarily muscle) according to a postreceptor defect. Finally the causes of insulin resistance in liver diseases are still not known.
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PMID:[Insulin resistance in liver diseases]. 353 94

The release of insulin and glucagon in cirrhotic rats was examined. Rats were made cirrhotic by a combination treatment of carbon tetrachloride (CCl4) and phenobarbitone. Liver cirrhosis was verified by histologic findings. Both basal and stimulated release of insulin from isolated pancreatic islets, in vitro, were decreased significantly in cirrhotic rats, as compared with control rats. Basal, but not stimulated, levels of glucagon, in vitro, were reduced significantly in cirrhotic rats. Circulating levels of plasma insulin, glucagon, glucose, bilirubin, and amylase levels were unaffected in cirrhotic rats when compared with control rats. There were no signs of pancreatitis. The results indicated that the release of insulin and glucagon is depressed in cirrhotic rats and in rats treated with phenobarbitone and CCl4. Clearance of circulating insulin and glucagon by the liver was apparently reduced, since circulating levels of insulin and glucagon were unaltered in all treated rats.
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PMID:Insulin and glucagon production in experimental cirrhosis. 354 4

In the fasting state the mean portal blood flow demonstrated by the pulsed Doppler system with the Octoson in liver cirrhosis (LC) patients (velocity (PV), 10.2 +/- 3.5 (mean +/- SD) cm/sec, 7.0 +/- 2.6 cm/sec/m2; flow (PF), 579 +/- 262 ml/min, 383 +/- 184 ml/min/m2 (n = 40)) was significantly lower than that in control subjects (PV, 21.2 +/- 5.2 cm/sec, 14.7 +/- 3.9 cm/sec/m2; PF, 966 +/- 344 ml/min, 667 +/- 220 ml/min/m2 (n = 40)). Food intake increased PV by 15% and PF by 15% in LC (n = 8) and increased PV by 56%, PF by 125% in controls (n = 8). Glucagon increased PV by 30% and PF by 52% in LC (n = 10) and increased PV by 50% and PF by 120% in controls (n = 8). Secretin increased PV by 44% and PF by 75% in LC (n = 9) and increased PV by 66% and PF by 142% in controls (n = 8). Vasopressin decreased PV by 42% and PF by 54% in LC (n = 9) and decreased PV by 48% and PF by 62% in controls (n = 8). Insulin, gastrin, and prostaglandin E1 had no effect in either group.
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PMID:Effects of food intake and various extrinsic hormones on portal blood flow in patients with liver cirrhosis demonstrated by pulsed Doppler with the Octoson. 354 85

To see whether foods with slower rates of digestion may benefit the metabolic abnormalities seen in cirrhosis, the same food, processed in two different ways, was fed to seven patients with cirrhosis. The breakfast of lentils processed by prolonged heating, to produce more rapid in vitro digestion, resulted in a significantly higher incremental rise in large neutral amino acid levels at 60 min (p less than 0.02) and a tendency for a more rapid rise in total amino acid concentrations by comparison with conventionally cooked lentils with slower in vitro digestion rates. After more rapidly digested lentils, incremental levels of branched-chain amino acids were also higher at 60 min (67 +/- 9, p less than 0.001) despite a greater overall insulin response. Comparable incremental amino acid areas after both meals suggested that the total amount of amino acids absorbed was not influenced by processing. Greater blood glucose, insulin, and gastric inhibitory polypeptide responses were seen after the more processed meal with no significant differences in pancreatic glucagon, entroglucagon, or neurotensin levels. Processing a food to alter the rate of digestion may therefore be used to manipulate amino acid, glucose, and endocrine responses in cirrhosis.
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PMID:Effect of modifying the rate of digestion of a food on the blood glucose, amino acid, and endocrine responses in patients with cirrhosis. 354 27

Elevated plasma ammonia level in hepatic cirrhosis has been attributed to a lack of conversion of enteric ammonia into urea or to its entry into systemic circulation via portasystemic shunting, or to both. It is exaggerated by excessive protein intake. Because hyperglucagonemia is well documented in cirrhosis and a protein meal is an effective glucagon secretagogue, plasma glucose, insulin, glucagon, and ammonia levels were determined in 50 cirrhotic patients after an overnight fast. Effects of a protein meal were also assessed in 20 of these patients. Plasma glucose was normal and remained unaltered after a protein meal. Insulin, glucagon, and ammonia levels were elevated, but only in patients with advanced liver dysfunction. Ammonia levels correlated significantly with glucagon (r = 0.61, p less than 0.001), but not with insulin or glucose levels. Insulin and glucagon levels rose after a protein meal in all patients and controls; whereas a significant rise in the ammonia level occurred only in decompensated cirrhotics. Elevation of the ammonia level was significantly correlated with fasting glucagon (r = 0.54, p less than 0.05), as well as with glucagon response (r = 0.65, p less than 0.01), but not with basal insulin or insulin response. Furthermore, the rise in ammonia level occurred too early to be accounted for by enteric generation. Finally, direct effects of glucagon administration on plasma glucose and serum ammonia were examined in 15 cirrhotic patients. Glucose response was significantly blunted in cirrhotic patients as compared with normal subjects, whereas serum ammonia rose promptly but only in cirrhotics, with maximum rise being noted in cirrhotic patients with advanced liver dysfunction. This study, therefore, suggests that hyperglucagonemia may contribute significantly to hyperammonemia in hepatic cirrhosis.
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PMID:Elevated plasma ammonia level in hepatic cirrhosis: role of glucagon. 388 8

To study the role of pancreatic beta-cell function in glucose intolerance and frank diabetes that sometimes develops in cirrhosis, the C-peptide response to a bolus IV injection of 1 mg of glucagon was measured in nine controls and in two groups of patients with cirrhosis. The first group comprised nine subjects with normal or high-normal fasting plasma glucose and no glycosuria; five of them had impaired glucose tolerance. The second group consisted of eight cirrhotics in whom frank diabetes had developed six to 48 months after the diagnosis of cirrhosis. They were characterized by fasting plasma glucose greater than 140 mg/dL and permanent glycosuria. No differences in the degree of liver impairment or portal-systemic shunting were observed between the two groups. Plasma glucose response to glucagon was similarly reduced in cirrhotic subjects. Basal C-peptide was high normal in patients with cirrhosis, and significantly increased in nondiabetic subjects. By contrast peak C-peptide levels and total C-peptide responses to glucagon were low normal in cirrhotics and significantly reduced in patients with cirrhosis and diabetes. In 14 patients the C-peptide response to a standard meal was also measured. It was significantly reduced in patients with cirrhosis and diabetes (six cases), as compared to cirrhotic subjects without diabetes. Peak C-peptide after IV glucagon significantly correlated with peak C-peptide after the meal (r = .927), or total C-peptide response to meal (r = .871). Impaired insulin secretion may add to insulin resistance in patients with liver cirrhosis, leading to the development of frank diabetes, characterized by fasting hyperglycemia and glycosuria.
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PMID:Pancreatic beta-cell function in cirrhotic patients with and without overt diabetes. C-peptide response to glucagon and to meal. 389 76

Low serum, cerebrospinal fluid, erythrocyte, muscle and bone Mg concentrations have been found in liver cirrhosis, indicating a Mg deficiency. Decreased intake, fat malabsorption, renal tubular acidosis and increased serum levels of aldosterone, growth hormone and glucagon could be the causative factors.
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PMID:Magnesium and liver cirrhosis: a hypothesis. 403 1


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