Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Development of diabetes mellitus is a common complication of side to side porta-caval anastomosis (PCA). Five patients with liver cirrhosis and portal hypertension have been studied with intravehous (IVGTT, 0,5 g/Kg B.W.) and oral (OGTT, 1 g/Kg B.W.) glucose tolerance tests before and three weeks after PCA. Fasting plasma glucose was 84 +/- 7 before and 87 +/- 3 mg/dl after PCA. Fasting IRI increased from 17 +/- 3 to 31 +/- 6 microU/ml. The pattern of plasma glucose and IRI response to IVGTT did not change after PCA. Plasma glucose resonse to OGTT after PCA showed only an earlier rise at 60 instead of 90 minutes, whereas IRI resonse (area under the insulin curve) was significantly enhanced (from 12.4 to 19.8 U/l, p < 0.05). These data suggest a role of gut polipeptides in determining hyperinsulinemia and insulin resistence in PCA patients.
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PMID:[Glucose tolerance and insulinemia in patients with hepatic cirrhosis and portal hypertension treated by portacaval anastomosis]. 39 34

To clarify the mechanism of hyperinsulinism of hepatic cirrhosis, plasma insulin and C-peptide levels before and after oral glucose loads were measured in 34 patients with cirrhosis, 15 patients with chronic hepatitis, and 25 normal subjects. While plasma immunoreactive insulin (IRI) levels during oral glucose tolerance testing (OGTT) were significantly increased in cirrhotics, plasma immunoreactive C-peptide (CPR) levels were elevated slightly. The C-peptide to insulin ratio throughout OGTT was significantly smaller in cirrhotics than in normal subjects (P less than 0.01). A decreased hepatic insulin degradation rate has been suggested to one of the main causes of hyperinsulinism in hepatic cirrhosis. The ratio of the difference between basal and 30-min CPR values and basal and 30-min OGTT blood glucose values [delta CPR: delta BS(30)'] as well as the delta IRI: delta BS(30') ratio was significantly decreased in cirrhotics (P less than 0.01). These results indicate that insulin secretion in response to a glycemic stimulus is reduced in cirrhotics. Both the ratios of the sums of six IRS and CPR values of OGTT (sigma CPR: sigma IRI) and delta CPR: delta BS(30') and sigma CPR: sigma BS(30') were found in inverse relationship with indocyanine green retention rate in cirrhotics.
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PMID:Degradation and secretion of insulin in hepatic cirrhosis. 40 Jul 32

Immunologically pure human transferrin type C (TfC) was isolated from the plasmas of 11 individual healthy donors. After conversion into the 2Fe-form, the preparations were analysed by polyacrylamide gel electrophoresis and chromatography on DEAE-cellulose. In all samples studied by either method the presence of three components, designated A, B and C, was observed. Calculations from eight chromatograms yielded the following relative proportions for the components: A:6%, B:62% and C:32%. The quantity of iron bound played no role in this chromatographic resolution. The components were immunologically identical but their sialic acid content increased inthe order of A less than B less than C. The presence of galactose as an ultimate residue of the oligosaccharide chains in TfC component A was confirmed by a biological test. This observation together with the results of earlier analyses for hexose, hexosamine and galactose in the subfractions from Behringwerke human transferrin, suggests that sialic acid is probably the only variable among TfC components A, B and C. Loss of sialic acid from component C during the isolation of TfC was excluded as an explanation for the presence of the other two components. The electrophoretic appearance of TfC samples from five patients with liver disease (chronic active hepatitis, cirrhosis or alcoholic liver) did not noticeably differ from that of TfC FROM HEALTHY PERSONS. Baboon transferrin resembles TfC with respect to sialic acid heterogeneity. This species was therefore studied to decide whether sialic acid is gradually lost from transferrin in the circulation or whether transferrin is not fully sialylated before discharge from the hepatocyte. Using DEAE-cellulose chromatography no difference was found between baboon transferrin molecules which were less than 6h old and those which had a mean age of 8.9 days. By inference it is suggested that the reason for the multiplicity of TfC is also likely to be biosynthetic.
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PMID:The molecular components of human transferrin type C. 40 68

Insulin degradation was measured by the C-peptide/insulin ratio in 19 patients with portal vein block with extensive spontaneous portal-systemic shunting but minimal liver cell damage: 13 patients with biopsy-proved cirrhosis and 12 controls. Blood obtained fasting and for 3 hr after oral glucose was assayed for glucose, insulin, and C-peptide. Fasting C-peptide and insulin levels in patients with portal vein block and those in controls did not differ. Eight of 13 cirrhotic patients had fasting hyperinsulinemia with a significantly reduced C-peptide/insulin ratio. After glucose administration, the C-peptide/insulin ratio in portal vein block patients with normal aspartate transaminase levels did not differ from control values. In portal vein block patients with elevated asparatate transaminase levels, the C-peptide/insulin ratio was significantly reduced only from 60 min onwards. All the cirrhotic patients showed a significantly reduced C-peptide/insulin ratio after glucose administration. It is suggested that portal-systemic shunting of blood in the presence of a normal liver does not influence hepatic insulin metabolism and that the hyperinsulinemia of cirrhosis is a feature of parenchymal liver damage. In addition, insulin degradation was abnormal in all cirrhotic patients at high insulin secretion rates, even when fasting insulin levels were normal.
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PMID:Effects of spontaneous portal-systemic shunting on insulin metabolism. 42 95

In 6 patients with cirrhosis of the liver and in 6 healthy controls the elimination half life of the serum leucine level (t 1/2 Leu) was determined after intravenous administration of 50 mg leucine per kg bodyweight. Examinations were repeated with simultaneous administration of 0,33 g glucose per kg bodyweight and during a continuous infusion of 500 microgram somatostatin over 60 minutes. The following results were obtained: 1. In cirrhotics and in healthy controls the t 1/2 Leu was shortened during the additional glucose administration compared with the t 1/2 Leu after leucine administration alone and was prolonged by inhibiting insulin secretion by somatostatin. 2. In spite of significantly higher serum insulin levels the t 1/2 Leu in patients with cirrhosis of the liver was significantly prolonged compared with healthy controls after leucine administration as well after leucine and glucose administration. Therefore we conclude, that in patients with cirrhosis of the liver in spite of elevated serum insulin levels leucine as well as glucose are metabolized slower. These results are indicating peripheral insulin resistance regarding the assimilation of glucose and leucine (at least in patients with portocaval shunts).
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PMID:[Intravenous leucine load in patients with cirrhosis of the liver (author's transl)]. 42 89

In 12 patients with liver cirrhosis (LC) and 11 normal subjects (N) equimolar (0.75 g/kg/h for 4 hrs.) 14C-(1)-glucose and 14C-(1)-fructose infusions were administered. When given fructose, N and LC showed only a small increase of serum-glucose and -fructose concentrations in steady state. In N and LC the total fructose clearance was significantly higher than the total glucose clearance. No differences were found between N and LC. The metabolic clearance was equal in both groups when given fructose, whereas during glucose infusion lower in LC than in N. 30% of the infused 14C-fructose were recovered in 14C-glucose. The renal loss in both groups was higher for glucose than for fructose. A more extensive renal 14C-excretion during infusion of 14C-fructose was due to a higher 14C-lactate excretion.
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PMID:[Fructose tolerance and utilization in healthy and chronically diseased liver]. 44 6

Plasma immunoreactive glucagon (IRG) was examined in volunteers with biopsy-proven cirrhosis of the liver after recovery from surgical portal--caval anastomosis. A wide range of increased total plasma IRG concentrations was found after overnight fast in groups of cirrhotic subjects with and without fasting hyperglycemia. Gel filtration chromatography of plasma showed a major component in the 3500-mol wt fraction in all cases so studied. Administration of glucose i.v. caused rapid suppression of total plasma IRG in normoglycemic and non-insulin-dependent hyperglycemic cirrhotic subjects. After administration of oral glucose, total plasma IRG was suppressed rapidly in normoglycemic cirrhotic subjects, while non-insulin-dependent hyperglycemic cirrhotic subjects exhibited delayed but prolonged suppression. Chromatography of selected plasma with glucose-suppressed total IRG showed a major decrease in the 3500-mol wt component in every case. Exaggerated increments of plasma gastric inhibitory polypeptide were demonstrable in both groups of cirrhotic individuals after administration of oral glucose, and it is speculated that this peptide may contribute to stimulation of glucagon secretion in liver disease associated with insulin deficiency.
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PMID:Hyperglucagonemia in liver cirrhosis with portal-systemic venous anastomoses: responses of plasma glucagon and gastric inhibitory polypeptide to oral or intravenous glucose in cirrhotics with normal or elevated fasting plasma glucose levels. 44 82

In 7 normals and 7 patients with cirrhosis of the liver the influence of moderate physical work on glucose turnover was determined with 14C-glucose. Under resting conditions glucose turnover was 0.60 +/- 0.12 mmol/h/kg in the normals and 0.45 +/- 0.13 mmol/h/kg in the patients (mean +/- SD). During one hour's ergometer work of 45 +/- 12 watt, an increase of 90 +/- 42% (normals) and 53 +/- 29% (patients) was observed which resulted in a significantly lower turnover in the cirrhotics during work (normals 1.12 +/- 0.16, cirrhotics 0.68 +/- 0.14 mmol/h/kg). Serum concentrations of glucose, insulin and FFA remained constant in the normals, while in the patients a slight decrease in glucose and FFA was observed. Serum lactate levels were slightly higher and normalization lasted longer than in normals. It is obvious from these results that even fundamental liver functions, such as glucose production, are disturbed in patients with liver cirrhosis and show a reduced augmentation during physical work.
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PMID:[The effect of light physical work on the glucose formation in the liver in patients with liver cirrhosis]. 45 99

Porphyria cutanea tarda (PCT) has a known increased incidence of diabetes mellitus and hepatic involvement. We investigated glucose tolerance and glucoregulatory hormone alterations in seven patients with PCT and correlated these results with hepatic histology by percutaneous liver biopsy. Abnormal glucose tolerance was observed in six of the seven patients (87%). Fasting serum insulin levels were normal range, and normal glucose and growth hormone responses to standard, exogenous intravenous insulin were observed. Fasting serum glucagon and urine free cortisol levels were normal in those patients in whom they were measured. While varying degrees of abnormalities were found on histopathologic exam of the liver biopsies, no patient met the criteria for cirrhosis, and none of the patients demonstrated abnormal levels of insulin counterregulatory hormones commonly seen in cirrhosis. Thus, liver disease may not be the sole cause of the observed glucose intolerance and hyperinsulinemia in PCT patients.
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PMID:Carbohydrate metabolism in porphyria cutanea tarda. 46 44

The present study was performed in order to evaluate the plasma glucose pattern in cirrhotic patients who, in the course of a continuous somatostatin infusion (500 microgram/h), were given pulses of glucagon (1 mg i.v.). In normal as well as in cirrhotic subjects somatostatin infusion provoked a marked reduction of the IRI plasma level and this was uninfluenced by subsequent glucagon administration. The rise in plasma glucose level in response to i.v. glucagon administration during somatostatin infusion was less marked in cirrhotics compared to normal subjects. This can be attributed to a variety of factors such as reduced number of liver cells or quantitative or qualitative changes of the liver cell glucagon receptors. Glucagon does not seem to contribute to the pathogenesis of carbohydrate intolerance in liver cirrhosis.
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PMID:Effect of somatostatin (SRIF) on plasma glucose and insulin response to glucagon in liver cirrhosis. 48 63


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