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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats after portacaval anastomosis (an animal model of chronic liver disease), transport of tryptophan and other members of the large neutral amino acid group from blood to brain was markedly enhanced. Increased transport activity was apparently restricted to the neutral amino acid transport system, since brain uptake of glucose, inulin, and tyramine was unaffected while blood-brain arginine transport was significantly reduced. These results strikingly confirm the hypothesis that carrier-mediated blood-brain transport is the limiting factor determining the availability of the neutral amino acids to the brain. The encephalopathy associated with cirrhosis may be the result of abnormal neurotransmitter metabolism and neurotransmission secondary to increased neutral amino acid transport activity and an increased brain content of members of the neutral amino acid group.
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PMID:Blood-brain neutral amino acid transport activity is increased after portacaval anastomosis. 66 19

Fuel homeostasis was studied in 15 patients with hepatic cirrhosis who previously had sustained upper gastrointestinal hemorrhage secondary to portal hypertension. By combining substrate arteriovenous concentration differences with measured hepatic blood flow rates, the exchange rates of metabolites across the liver was calculated. Hepatic extraction of acetoacetate, beta-hydroxybutyrate, lactate, pyruvate, analine, and glycerol was studied. After an overnight fast, splanchnic glucose production in 15 cirrhotic patients was diminished markedly. Despite reduced total glucose production, there was no decrease in hepatic gluconeogenesis; instead, there was increased glucose formation from amino acids, glycerol, lactate, and pyruvate. In patients with hepatic cirrhosis, the liver does not produce as much glucose as does a normal liver; the failing cirrhotic liver is capable of maintaining fuel homeostasis by increased ketone-body production.
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PMID:Hepatic metabolism in patients with alcoholic cirrhosis. 66 24

Immunoreactive insulin level proved to be elevated in the blood serum on fasting stomach and at various periods after glucose administration in patients with cirrhosis of the liver with normal glucose tolerance. Reduced insulin sensitivity of the isolated adipose tissue was observed in patients with cirrhosis of the liver. The blood serum cortisol level in these patients failed to differ from such in healthy persons; that calls in doubt participation of this contrinsular hormone in the genesis of reduced insulin sensitivity in chronic diseases of the liver. Elevation of peripheral insulin resistance can promote development or detection of carbohydrate metabolism disturbances in patients with chronic diseases of the liver.
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PMID:[Sensitivity of isolated adipose tissue to insulin and questions concerning the pathogenesis of diabetes mellitus in patients with chronic liver diseases]. 72 82

Basal and reactive peripheral hyperinsulinism recorded in alcoholic hepatic disease may result from decreased hepatic breakdown or pancreatic hypersecretion. C-peptide (CPR) and insulin (IRI) concentrations were measured in 3 groups of 8 alcoholic patients--steatosis, compensated and decompensated cirrhosis--and compared with 8 normal subjects in order to determine the importance of these two possibilities. At basal state, the molar ratio CPR/IRI was near the normal (8.7 +/- 0.9) but is diminished in the 8 hyperinsulinaemic patients (5.9 +/- 0.6). After i.v. glucose tolerance test and tolbutamide stimulations, an hyperreactivity of IRI and CPR may be noted in cirrhotics. A relative insensitivity of the B-cell to glucose appeared after comparison with the effect of tolbutamide. Thus basal hyperinsulinism resulted of decreased hepatic breakdown and stimulated hyperinsulinism resulted of hypersecretion. Glucose intolerance and anomalies of the insulin secretion were more apparent with severe hepatic disease.
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PMID:[Insulin secretion in alcoholic hepatopathy: analysis by measurement of C-peptide (author's transl)]. 73 68

Circulating insulin was determined by radioimmunoassay in ten children with cirrhosis of the liver and in 6 age-matched controls. They were found to be elevated in cirrhotics during fasting as well as at 1/2, 1, 1 1/2 and 2 h during the oral glucose tolerance test. These determinations were also carried out in two children with extrahepatic portal hypertension to show the possible role of portal systemic shunts for the elevated serum insulin levels. We believe that the hyperinsulinemia of these patients was related to decreased insulin degradation by the liver as well as to portal-systemic shunting.
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PMID:Hyperinsulinemia in childhood cirrhosis. 73 3

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
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PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

Glucagon is secreted not only by A2-cells of the pancreatic islets but also by A cells in the gastric fundus and duodenum. Several reports have demonstrated that the glucagon plasma concentration is increased in genetic diabetes as well as in many conditions associated with a decreased glucose tolerance such as hepatic cirrhosis, myocardial infarction, infectious diseases, burns, taumatic shock, glucagonomas, acute pancreatitis, acromegaly, pheochromacytoma and Cushing's syndrome. Hyperglucagonemia is particularly important in diabetic ketoacidosis and in non-ketotic hyperosmolar coma. The mechanisms responsible for the diabetic's hyperglucagonemia remain controversial. According to several authors, the increased glucagon secretion is, for its main part, secondary to a prolonged defect in insulin secretion and thus relatively insensitive to an acute insulin administration. According to others, the A cell abnormality is of primary origin, independant from insulin deficiency and its effects are cumulative with those of the insulin lack. Several reports dealing with induced or spontaneous experimental diabetes are in favor of the first or the second hypothesis. It appears likely that glucagon plays a role in the metabolic derangments of diabetes. Indeed, hepatic glucose production is closely related to the ratio of molar concentrations of insulin and glucagon. Finally, in insulin-dependant diabetics, somatostatin infusion reduces plasma glucagon concentration and blood glucose and prevents the development of ketosis after withdrawal of insulin therapy. These results illustrate the contribution of glucagon in the pathogenesis of hyperglycemia and ketosis. Several arguments have been accumulated in favor of the following concept: diabetes hyperglycemia results both from glucose under-utilization secondary to insulin lack and from hepatic glucose over-production due to glucagon excess. Although controversial, the role of glucagon in ketogenesis appears likely.
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PMID:[The role of glucagon in hyperglycemia. A review (author's transl)]. 79 28

Various parameters of the insulin secretion in man may be appreciated and calculated by studying the insulin response to an intravenous pulse of glucose followed 120 minutes later by one of tolbutamide. The relative insensitivity of the B cell to glucose, probable marker of a constitutional pancreatic predisposition to diabetes may be assessed in a given individual whatever his age and body weight. The glucose intolerance per se is due to, or accompagnied by various B cell dysfunctions according to its etiology. This is illustrated by the results observed in chronic pancreatitis, liver cirrhosis, aged or obese subjects.
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PMID:[A method of studying insulin secretion in humans: the glucose stimulation test, followed by tolbutamide]. 79 23

Most forms of liver disease are probably associated with impaired gluconeogenesis, although hypoglycaemia is rarely an important clinical feature. Blood concentrations of the gluconeogenic precursors, lactate, glycerol and alanine are elevated although, in certain situations, alanine levels may be decreased. Abnormal glucose tolerance is present in both acute and chronic liver disease, but is usually not of clinical importance. The mechanism of glucose intolerance remains uncertain, with diminished hepatocyte mass, portal diversion and insulin resistance the major postulates. Indeed, the importance of the liver in disposing of an oral glucose load, is still questioned. Both hyperinsulinism and hypoinsulinism are found in liver disease, with hyperinsulinism common in cirrhosis and acute viral hepatitis. This is accompanied by insulin resistance. The hyperinsulinism is probably due to defective hepatic clearance of insulin rather that to over-production. The cause of the insulin resistance remains to be established. Glucagon levels are raised and may contribute to this resistance. Growth hormone levels are also increased but are associated with low somatomedin levels and the role of growth hormone in insulin resistance is therefore questionable. Future developments include use of new animal models, studies of biopsy specimens and studies of hepatic hormone receptors.
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PMID:Carbohydrate metabolism in liver disease. 79 84

Oral glucose tolerance tests (100 g glucose) and the intravenous tolbutamide test were carried out. The glucose tolerance was seen to be disordered even in acute infectious hepatitis, but returning to normal when cured. If chronic hepatitis develops, however, the proportion of manifest diabetes increases to 7.2% in chronic persistent hepatitis and to 16.3% in chronic progressive hepatitis, while 30% each have latent diabetes. The glucose tolerance is most impaired in fatty liver (stage III) and in active cirrhosis of the liver with portal hypertension, where more than half of all patients present manifest or latent diabetes. Conversely, glucose tolerance improves even in chronic hepatitis and in cirrhosis of the liver as the inflammatory activity subsides. The main cause for the development of "liver diabetes" is therefore likely to be the activity of the inflammatory process, the extent of portal hypertension, disorders of glucose regulation in the liver and the increased insulin inactivation in the cirrhotic liver.
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PMID:[Disorders of glucose tolerance in 2600 histologically confirmed acute and chronic liver patients (author's transl)]. 81 Jun 95


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