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

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

Derangements in glucose, amino acid and protein metabolism in patients with liver cirrhosis were examined with special reference to plasma levels of human growth hormone (HGH). Changes in blood glucose, IRI (immunoreactive insulin), HGH, FFA (free fatty acid) and plasma free amino acid levels were determined in controls and patients following either oral glucose load, protein feeding or intravenous arginine infusion. 1) In patients with liver cirrhosis, incidence of glucose intolerance after glucose tolerance test (GTT) was high and IRI levels were elevated in the fasting state as well as after glucose, protein or arginine loads. 2) Fasting levels of blood HGH were significantly higher in liver cirrhosis than in controls. GTT revealed that blood HGH levels decreased slightly during the rising phase of blood glucose, and conversely, increased during the falling phase of glucose (180 minutes after the glucose load) both in controls and in patients. In cirrhotic patients, marked increases in HGH levels were observed both 120 minutes after the protein load and 60 minutes after the arginine infusion. 3) Fasting levels of serum FFA were significantly higher in liver cirrhosis than in controls. Both controls and patients, however, showed a similar pattern of change in FFA levels following GTT or protein ingestion, i.e. a minimum value 120 minutes after the load and a gradual increase thereafter. 4) Fasting levels of plasma free amino acids were significantly higher in cirrhotic patients than in controls. After the glucose load, however, slight decrease was noted in some amino acid levels. All the amino acid levels examined were elevated following protein ingestion, particularly in cirrhotic patients. 5) A positive correlation was demonstrated in cirrhotic patients between total plasma free amino acids and maximal HGH responses following protein ingestion. Similar significant correlations were observed between the maximal HGH response and the plasma level of several amino acids such as His., Ser., Gly., Thr., Ala., and Ileu., respectively. 6) In cirrhotic patients, negative correlations were demonstrated between fasting levels of serum albumin and total plasma free amino acids or maximal HGH responses, respectively, after the protein ingestion. From these results it was inferred that derangements in the metabolism of protein and amino acids in cirrhotic patients may result in an increase in plasma free amino acid level which in turn stimulates HGH secretion. It was surmised that the HGH levels so elevated in the patients may cause FFA mobilization which in effect results in the glucose intolerance.
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PMID:[Studies on glucose, amino acid and protein metabolism in patients with liver cirrhosis in relation to plasma levels of human growth hormone (author's transl)]. 81 50

The cholesterol-lowering effect of portacaval anastomosis in homozygous familial hypercholesterolemia suggested a study of lipid metabolism in cirrhotic patients after portasystemic anastomoses. Fasting serum cholesterol, triglycerides, insulin, and glucagon levels were obtained in 20 patients with alcoholic cirrhosis and portacaval anastomosis, and in 21 nonshunted subjects with cirrhosis. After 100 g of glucose, given orally, insulin and glucagon levels were measured. In the shunted patients serum cholesterol was higher than in the nonshunted subjects, 240 +/- 15 mg per 100 ml (mean +/- 1 SEM) versus 180 +/- 13 mg per 100 ml, P less than 0.01. Triglycerides were normal in both groups. Fasting insulin was elevated to a greater extent in the shunted patients with cirrhosis (36 +/- 5 muU per ml) than in the nonshunted patients (22 +/- 4 muU per ml), P less than 0.05. Two hours after glucose, insulin levels were also elevated to a greater extent in the shunted subjects (304 +/- 50 muU per ml) than in the nonshunted subjects (167 +/- 29 muU per ml), P less than 0.03. Fasting glucagon (corrected for interference factor) was elevated to a greater extent in the shunted subjects (204 +/- 35 pg per ml) than in the nonshunted subjects (80 +/- 19 pg per ml), P less than 0.01. The explanation for serum cholesterol elevation after surgical shunting in cirrhotics is unknown. Two possible hypotheses--the differential action of insulin and glucagon on cholesterol metabolism and the effects of shunting on the cirrhotic liver--are discussed.
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PMID:Serum lipids, insulin, and glucagon after portacaval shunt in cirrhosis. 83 May 79

Statistically there exists an increased coincidence between liver cirrhosis and diabetes mellitus. The higher frequency of cirrhosis in diabetics compared with the normal population is to be explained partly from the higher risk of hepatitis. In addition to this the diabetic suffers from disturbances which further the development of cirrhosis, such as fatty degeneration of the liver, abuse of alcohol, more frequent inflammatory diseases of the bile duct and others. When a diabetes mellitus exists in liver cirrhosis it is to be differed between a diabetes due to absolute or relative insulin deficit and disturbances of carbohydrate clearance which are associated with normal or increased insulin levels. The latter form can be denoted as so-called liver diabetes. Main cause of this carbohydrate intolerance is an insulin resistance, partly by deminution of the metabolically active liver parenchyma, partly by the diminished reactivity of the peripheral tissues. By prophylactic measures and differentiated therapy may be favourably influenced lesions of the liver in diabetes mellitus as well as disturbances of the carbohydrate metabolism.
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PMID:[Liver cirrhosis and diabetes mellitus]. 85 43

Peculiarities of clinical picture of diabetes mellitus in its combination with chronic hepatitis and cirrhosis of the liver were studied in 60 patients. Diabetes mellitus developed mostly against the background of chronic affection of the liver, preceding it. Glucose tolerance disturbances according to the type of latent and manifest diabetes were revealed in 28% of 132 patients with chronic hepatitis and cirrhosis of the liver. Histological study of the pancreas in 63 patients who died of cirrhosis of the liver demonstrated marked fibrosis of hepatic parenchyma without any noticeable changes in the pancreatic islets. The blood insulin and growth hormone levels were significantly greater in 132 patients examined than in healthy persons. The mentioned changes in the glycemia level, of the insulin and growth hormone level after glucose administration were more pronounced in cirrhosis of the liver than in chronic hepatitis, and in late stages of portal cirrhosis than at its early stages. The leading role played by insulin sensitivity reduction of the peripheral tissues in the pathogenesis of carbohydrate metabolism in cases with chronic diseases of the liver is supposed.
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PMID:[Clinical picture and pathogenesis of diabetes mellitus in chronic hepatitis and cirrhosis of the liver]. 90 62

Blood sugar, insulin and GH values were examined in two groups of cirrhosis of the liver patients, with and without ascites, after the administration of 100 g glucose per os. No significant differences between the two groups were observed. Insulin values were higher than those in the controls, with a pattern similar to that noted in subjects with chemical diabetes. GH values were higher than in normal subjects and secretion was not suppressed.
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PMID:[Plasma insulin and GH during oral glucose load in liver cirrhosis]. 95 Oct 48


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