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

Cirrhosis is complicated by numerous abnormalities of carbohydrate metabolism although these are seldom of clinical importance. Carbohydrate intolerance is extremely common and is accompanied by hyperinsulinaemia, hyperglucagonaemia and elevated levels of gluconeogenic precursors. The hyperinsulinaemia results from impaired hepatic degradation of insulin while recent evidence suggests that pancreatic hypersecretion is responsible for the elevated levels of glucagon in cirrhosis. The role of hepatocellular damage and portal-systemic shunting in the pathogenesis of these abnormalities is controversial but the derangements in carbohydrate metabolism probably reflect hepatocellular damage rather than portal-systemic shunting.
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PMID:The glucoregulatory hormones in cirrhosis of the liver. 47 36

After summing up existing theories about the origins and development of functional hepatic encephalopathy, the authors report on the effects of six-hour intravenous infusions of ornithine alphaketoglutarate (60 g dissolved in 500 ml distilled water), administered to 10 patients with ethylic hepatic cirrhosis in conjunction with a normal protein intake (70 g/day). Arterial blood ammonemia, venous blood aminoacidemia and the insulin/glucagon ratio did not vary during or after infusion. This method of treatment therefore seems to meet the protein requirements of these undernourished patients.
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PMID:Effects of ornithine alphaketoglutarate on blood insulin, glucagon and aminoacids in alcoholic cirrhosis. 48 88

Twelve patients with liver cirrhosis and ten normal subjects were studied. Using a constant intravneous infusion of glucose, insulin and somatostatin over 2 1/2 hours we determined the stteady state plasma glucose level (SSPG) in order to measure insulin resistance. The results demonstrated that the cirrhotic patients were insulin resistant compared to normals and that plasma glucagon does not account for the insulin resistance in these patients.
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PMID:Glucose, insulin and somatostatin infusion for the determination of insulin resistance in liver cirrhosis. 52 Oct 9

The effect of liver disease on glucagon metabolism was examined in nine patients with chronic liver disease who were studied both before and after the creation of a surgical portasystemic shunt. Hepatocellular function did not deteriorate after shunt surgery. However, hepatic perfusion with splanchnic venous blood, as determined by scintisplenoportography, decreased after shunt surgery in six subjects but appeared unaltered in three. Basal plasma immunoreactive glucagon (IRG) levels in the pre-shunt cirrhotic group were significantly greater (p <0.005) than in control subjects and further increased (p <0.05) after shunt surgery. Moreover, the increase in basal IRG after shunt was evident only in patients in whom portasystemic shunting was demonstrably increased by surgery. Despite the higher basal IRG levels postoperatively, shunt surgery in the cirrhotics did not alter basal glucose and insulin levels or the glucose and insulin response to a glucose or protein load. Circulating IRG was heterogeneous in the pre-shunt cirrhotic patients: the 9000 molecular weight fraction comprised 27+/-4%, the 3500 mol. wt. fraction 71+/-4%, and the > 40 000 mol. wt. fraction was minimal. After shunt surgery, the relative proportion of the 9000 mol. wt. fraction of IRG (13+/-3%) decreased significantly (p <0.05) and this fall was associated with a corresponding increase in the 3,500 mol. wt. fraction (84+/-4%). It is concluded that, in cirrhosis, hyperglucagonaemia is: (1) dependent on the degree of portasystemic shunting rather than impaired hepatocellular function; (2) predominantly due to increased circulating 3500 molecular weight glucagon; and (3) not a major factor in the pathogenesis of carbohydrate intolerance in liver disease.
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PMID:Effect of portasystemic venous shunt surgery on hyperglucagonaemia in cirrhosis: paired studies of pre- and post-shunted subjects. 53 93

The effect of fructose infusions (1.0 g/kg/g) on serum glucose, insulin, lactate, free fatty acids, glucose production and glucose oxidation was investigated with 14C-glucose in 10 normals and 11 patients with liver cirrhosis. Elevation of glucose and insulin were small and only slightly higher in cases of cirrhosis. Decrease of free fatty acids and rise of lactate were approximately the same in both groups. During infusion of fructose glucose turnover increased up to 196 +/- 41% in the normals and up to 279 +/- 78% in the patients with cirrhosis. No influence on the specific activity of 14CO2 was observed. It was therefore suggested, that approximately the same amount of glucose leaving the liver in excess during infusion of fructose was taken up by the liver at the same time. This behaviour of glucose supply to the blood stream and removal from it would explain, why high rates of conversion of fructose to glucose were measured with 14C-fructose, while only small amounts of glucose production were estimated from hepatic arteriovenous differences.
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PMID:[The effect of fructose on glucose formation and oxydation in healthy subjects and patients with liver cirrhosis]. 56 17

In 11 normal subjects (NS) and 12 patients with liver cirrhosis (LC) the utilisation of 14C-glucose and 14C-fructose infusions (0.75 g/kg/h for 4 h) was compared. There were nor relevant side effects. Lactate and pyruvate were in both groups during fructose infusion slightly increased compared to glucose infusion. The free fatty acids were significantly decreased. The serum glucose level rose more in LC than in NS when given fructose infusion. During glucose and fructose infusion in LC higher insulin concentrations were calculated than in NS. 15 min after infusion of 14C-fructose 20% of the total serum activity was 14C-glucose, after 2 to 4 h the level was 30%. Differences between NS and LC were not found to be significant. The specific activity of 14CO2 was the same in both the 14C-glucose infusion and the 14C-fructose infusion. The glucose oxidation was impaired in LC, but not the 14CO2-exhalation during infusion of 14C-fructose. Unimpaired 14CO2-exhalation, and normal utilisation and conversion to glucose are arguments for the use of fructose in infusion treatment of cirrhotics.
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PMID:[Comparative studies on the use of equimolar 14C-labeled glucose and fructose infusions in normal subjects and patients with liver cirrhosis]. 57 38

It is evident that ethanol by itself or one of its metabolites produces alterations in transport, metabolism and disposition of carbohydrates. Ethanol acts via changes in the redox state of co-factors; e.g. ethanol-induced hypoglycemia is due, partly, to the inhibition of hepatic gluconeogenesis by ethanol as a consequence of the increased NADH2/NAD ratio in patients whose glycogen stores are already depleted. On the other hand, hyperglycemia has also been described in patients with alcoholism. Although its mechanism is still obscure, abnormal hormonal secretion of insulin, catecholamines and glucocorticoids has been incriminated. Finally, structural changes of the liver and pancreas such as cirrhosis and pancreatitis produced by chronic alcohol consumption should also be considered as pathogenetic factors in a variety of clinical states involving deranged carbohydrate metabolism.
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PMID:Alcohol induced changes of carbohydrate metabolism [author's transl]. 70 66

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


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