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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatic regeneration in partially hepatectomized, eviscerated rats, and survival in mice infected with lethal doses of murine hepatitis virus, are both strikingly promoted by combined administration of insulin and glucagon. These two hormones, although potent promotors, fail as initiators of hepatocyte proliferation in animals with intact liver, which suggests a requirement for additional factors, probably derived from non-portal-splanchnic organs. We now find that continous intraperitoneal infusion of epidermal growth factor (EGF) initiates DNA synthesis, as determined by incorporation of [3H] thymidine, in livers of adult rats in vivo. The rise in DNA labelling, which is small with EGF alone, is augmented by addition to the infusion of either glucagon or insulin. This is in agreement with reports on adult hepatocytes in culture. Whether EGF has a physiological role in regulating liver growth under normal conditions in vivo remains to be determined.
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PMID:Hormonal factors concerned with liver regeneration. 30 14

Intravenous glucose tolerance tests were performed in 10 patients with acute virus hepatitis. The assimilation coefficient of glucose and the level of insulin and C-peptide in serum were determined before and in the course of the glucose tolerance tests. In comparison to healthy normal weight persons C-peptide concentration in patients with acute hepatitis increased twice as high whereas the pattern of insulin secretion did not differ significantly. The higher levels of C-peptide indicate an increase of the beta-cell secretion in acute hepatitis. One could suppose an increased hepatic destruction of insulin in acute hepatitis, because there is no significant difference among the insulin levels. More likely, there is a reactive increase of secretion of the beta-cell due to a reduction of insulin sensitivity and this is indicated much better by C-peptide- than insulin levels because of the longer half live of the the C-peptide molecule.
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PMID:[Concentration of C-peptide and insulin in serum of patients with acute virus hepatitis (author's transl)]. 36 78

The nitrogen metabolism in rats with toxic affection of the liver caused by administration of CCl4 was studied as affected by the amino acid mixture moriamine S-2. It is established that with toxic hepatitis the nitrogen metabolism is sharply disturbed, especially during protein deficiency. The following evidences for this fact: a rise in the depth of the nitrogen negative balance, an increase in the intensity of amine nitrogen and ammonia excretion with urea as well as an increase in the amount of amine nitrogen in blood and tissues with a simultaneous decrease in the content of protein. The parenteral administration of the amino acid mixture for eight days to the animals with a toxic affection of the liver is more effective when nitrogen preparation is combined with the group B vitamin, vitamin C, insulin, nerobolyl and sirepar.
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PMID:[Correction of nitrogen metabolism in rats with toxic hepatitis by parenteral administration of an amino acid mixture]. 42 34

Six to 12 hr after IP injection of 400 mg/kg of D-galactosamine in rats a 5-fold increase in plasma insulin was observed. In addition, impaired glucose assimilation was present after an IV Load in spite of unchanged fasting glucose levels. In streptozotocin-diabetic rats (100 mg/kg IV) plasma insulin remained diminished 12 h after induction of D-galactosamine hepatitis. Under identical conditions of preparation and incubation, the liver plasma membranes of D-galactosamine-treated rats, in both normal and diabetic states, bound only 40--60% as much insulin per mg of membrane protein as those of the control rats. Scatchard analysis suggested that this was due to a decrease in the number of receptor sites in the membranes of the D-galactosamine-injected rats. No difference in the insulin degrading capacity and in insulin-receptor dissociation of the plasma membranes between control and D-galactosamine-treated groups was found. These data suggest that a reduction in the number of hepatic insulin receptors in galactosamine hepatitis can lead to insulin resistance and hyperinsulinaemia.
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PMID:Reduced insulin binding to hepatic plasma membranes in D-galactosamine-treated rats. 48 65

In a 64-year old woman with a histologically confirmed Au-SH antigen negative acute virus hepatitis with an otherwise normal course, an extreme hypoglycemia lasting four days developed in the florid stage, and was treated with intravenous glucose drips. In spite of the supply of 130 g/24 hrs glucose on the 2nd day of hypoglycemia, the fasting blood sugar level next morning was 0 mg% ("aglycemia"). The hypoglycemia ran a course without autonomic or psychoneurological symptoms. As the hepatitis regressed, the carbohydrate metabolic disorder regained its equilibrium. It is assumed that this was a hepatogenic hypoglycemia. This may have reduced the glycogen reserves in the liver, also partly as a result of minimal diet, disturbed the gluconeogenesis and glycolysis and slowed the breakdown of insulin.
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PMID:[Hypoglycemia - aglycemia in virus hepatitis (author's transl)]. 80

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

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

The frequency of antibodies to the hepatitis B surface antigen was determined in 406 diabetics in two study series separated in time (1971-1972 and 1974-1975). In the 1971-1972 series, the antibody frequency in insulin and orally treated patients was significantly higher, and the incidence of hepatitis was also greater. The decline in the antibody frequency in the 1974-1975 series is primarily attributed to improved hygienic measures. Anti-HBs was more frequently demonstrable in insulin-dependent diabetics than in orally treated patients. Since the duration of diabetes was about three times as long in this treatment group and the frequency of metabolic checks twice as great, the raised antibody frequency in insulin-injecting diabetics was attributed to greater exposure to the virus.
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PMID:Antibodies against the hepatitis B surface antigen in diabetics. 85 42

Diabetes mellitus was tentatively diagnosed in a black-footed ferret with polyuria, polydipsia, polyphagia, dehydration, and weight loss. Laboratory findings (marked hyperglycemia (724 mg/100 ml), glycosuria, and ketonuria) and the subsequent favorable response to insulin therapy confirmed the diagnosis. Although lesions were not observed in the pancreas, gross and histologic findings concomitant with diabetes mellitus included arteriosclerosis, with calcification of the aorta and other major vessels; mild necrotizing hepatitis; and mild proliferative glomerulonephritis. A perineal adenocarcinoma, with metastasis to an internal iliac lymph node, was an incidental finding. Special stains demonstrated adequate numbers of beta cell granules in the islets of Langerhans. Thus, the diabetes was apparently due to a lack of release of the synthesized insulin or to diminished effectiveness of the secreted insulin.
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PMID:Diabetes mellitus in a black-footed ferret. 92 62

Within six months, acute viral hepatitis, type B, developed in three individuals associated with a nursing home in Denver. This attack rate, 1.4 cases per 100 patients and employees, was apparently higher than the reported incidence of hepatitis B in Denver during the same period. Parenteral inoculations could not be implicated as the means of acquiring hepatitis B. However, two of the hepatitis patients had had sexual contact within six months before their illness with an employee who was an insulin-dependent diabetic and a symptomatic carrier of HB-Sg. In addition, anti-HB-S antibodies were detected in his homosexual roommate. Although the chronic carrier was a food-handler, a seroepidemiologic survey of the employee population showed no spread of HB-Sag by means of food or casual contact. Only 1 (4.6%) of 22 employees tested had anti-HB-S antibodies. These results suggest that household and, in particular, sexual contact with a symptomatic HB-SAg carrier may be an effective nonparenteral or inapparent parenteral mode of transmitting HB-SAg.
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PMID:Hepatitis B and the HB-SAg carrier. An outbreak related to sexual contact. 117 69


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