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

Steatohepatitis (fatty liver hepatitis), histologically identical to alcoholic disease, occurs in some obese patients after jejunoileal bypass. A similar lesion occurs rarely in obese patients without bypass surgery, but the risk factors are poorly understood. Hepatic steatosis, steatohepatitis and fibrosis were sought in 351 apparently nonalcoholic patients at autopsy and various risk factors were evaluated. Incidence of steatosis and steatohepatitis correlated with the degree of obesity. Steatohepatitis was found in 18.5% of markedly obese patients and 2.7% of lean patients. Additional risk factors for steatohepatitis were type II diabetes, weight loss in the preterminal period shortly before death and intravenous glucose therapy in the last week of life. Severe fibrosis was found in 13.8% of markedly obese patients and in 6.6% of lean patients; this difference was largely explained by the higher prevalence of diabetes in obese groups. The risk factors defined in this study are known to be associated with abnormalities of free fatty acid metabolism. Obesity, type II diabetes and intravenous glucose therapy are associated with hyperinsulinemia, which may inhibit fatty acid oxidation. Obesity and weight loss increase the presentation of fatty acids to the liver. Similar metabolic changes may occur in obese patients after jejunoileal bypass surgery. Thus this study supports the hypothesis that fatty acids have a role in the hepatocellular necrosis found in some obese individuals.
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PMID:Fatty liver hepatitis (steatohepatitis) and obesity: an autopsy study with analysis of risk factors. 222 7

Chronic contamination of rats with heliotrin causing the development of hepatitis or hepatocirrhosis and partial hepatectomy to decrease the amount of liver cellular elements resulted in intolerance to glucose, a decrease in the sensitivity of the body to insulin, hyperinsulinemia after a glucose-tolerance test. The content of glycogen in the liver of the heliotrin contaminated rats was much lower than that in the controls and after glucose-tolerance an absolute increment of glycogen in the controls was 8.8-fold higher than in the heliotrin-contaminated rats. It was concluded that a decrease in glucose-tolerance and hyperinsulinemia in patients with chronic hepatitis and hepatocirrhosis were determined by a decrease in the amount of functionally active liver cellular elements and the development of insulin resistance.
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PMID:[Causes of hyperinsulinemia and decreased sensitivity to insulin in liver damage]. 352 17

6 girls, aged 4-16 years, with acanthosis nigricans and hirsutism were studied. Fasting and postglucose hyperinsulinism was present in the 5 older girls. In the youngest, a transitory diabetes with hyperinsulinism was induced by a cortisone therapy for hepatitis. Insulin resistance, suggested by the failure to significantly decrease blood glucose after insulin injection (0.1 U/kg), was demonstrated in three steps: (1) Patient plasma failed to bind 125I-insulin after a 5-day incubation followed by precipitation by antihuman globulin serum. (2) Specific 125I-insulin binding to rat liver membranes was identical in the presence of patient plasma and control plasma. (3) Specific 125I-insulin binding to the erythrocytes of the 6 patients (3.5-7.0%) was significantly lower (p less than 0.01) than in controls (4.5-19.5%). Moreover, the significant correlation present in controls between total binding and reticulocyte counts (r = 0.824, p less than 0.001) was absent in the patients. These data demonstrate further that, in the juvenile type of acanthosis nigricans, insulin resistance which may precede hyperinsulinism is not related to anti-insulin antibodies nor to antireceptor antibodies, but results from a primary defect of insulin receptors.
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PMID:Insulin-specific binding to erythrocytes in 6 girls with acanthosis nigricans. 648 30

Genetically obese mice (C57BL/6J-ob/ob), fed ad libitum, demonstrated a precipitous increase in the spontaneous death rate after 50 weeks. The first signs of morbidity were a ruffled hair coat and a progressive motor ataxia. Necropsy revealed that obese mice had pale and fatty livers, urolithiasis and grossly distended bladders. Microscopically, the hepatocellular changes observed in all aged obese mice included: a loss of orientation of hepatocytes, an enormous variability in the size of both hepatocytes and their nuclei, and an extensive deposition of both large and small lipid droplets, confirmed by an increase content of triacylglycerols. A subacute-to-chronic, multifocal, necrotizing hepatitis was also present. Kidneys from aged obese mice contained hypertrophied glomeruli and increased PAS-stained material. Tubular dilation with compaction of the tubular cells was also seen. There were no significant alterations in the microanatomy or mineralization of femurs from obese mice, yet there was a significant increase in plasma alkaline phosphatase activity. In obese mice at 62-63 weeks of age, hyperglycemia was present even in spite of hyperinsulinemia. Pituitary immunoreactive ACTH and its molar ratio to pituitary immunoreactive beta-endorphin were also increased in obese mice at this age. Even though the etiology of the decreased lifespan of genetically obese mice remains uncertain, the possibility is discussed that an overall defect in the central nervous system may be involved.
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PMID:Hormonal, metabolic and morphologic studies of aged C57BL/6J obese mice. 673 67

Twenty-one viral hepatitis patients underwent i.v. glucose tolerance tests during the acute phase of the illness. The results, expressed as the constant of glucose disappearance (Kg), were compared with those of 10 healthy control subjects. When the patients were grouped according to Kg-less than 0.9 or greater than 1.2 min-1-it was found that eight showed a delayed glucose disappearance together with a moderate hypoinsulinemic response (pattern 1). Another eight showed a normal glucose disappearance together with a hyperinsulinemic response (pattern 2). Five patients had intermediate Kg values. High levels of plasma free fatty acids (FFA) were a consistent finding in all patients, indicating that unrestrained lipolysis is an important feature of hepatitis. The extent of decrease in plasma FFA in response to the glucose load was markedly lower in all hepatitis patients than in the control subjects; the rate of decrease was most delayed in the pattern 1 patients. This suggested that the increased FFA availability is an expression of adipose tissue insulin resistance, which, in contrast to glucose disappearance, remains uncompensated by the relative hyperinsulinemia. It may contribute to the diminished peripheral glucose utilization, particularly in pattern 1 patients. We conclude that the different patterns of response in hepatitis may be discerned in one patient group by extending the diagnostic criteria of the glucose tolerance test. In addition to the differences in the magnitude of the peripheral insulin resistance, the main distinction between the two patterns lies in the capacity of the pancreas to adjust insulin secretion in order to maintain normal glucose homeostasis.
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PMID:Patterns of glucose intolerance and free fatty acid behavior in viral hepatitis. 700 83

To determine a possible relation of hepatic oxidative activity to glucose metabolism, the rates of oxygen consumption of liver slices from patients with chronic liver diseases were polarographically measured. The livers from patients with chronic (persistent and aggressive) hepatitis and with normal glucose tolerance showed almost the same respiratory activity as those from patients with normal livers and normal glucose tolerance, whereas the livers from patients with chronic hepatitis and with diabetic glucose tolerance (ie, diabetes mellitus secondary to chronic hepatitis) showed only a half the normal level. The decreased rate of respiration was also observed in liver slices from cirrhotics with glucose intolerance. The decrease in respiration was found in patients with normal or hyperinsulinemia as well as hypoinsulinemia responding to oral glucose load. No liver tests so far examined, except the oral glucose tolerance test, correlated with hepatic respiratory activity. It is concluded that in patients with chronic liver diseases the defect of liver respiration has a close relation to the glucose metabolism and is not necessarily associated with histological change of the liver.
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PMID:Glucose tolerance and respiratory activities of human liver biopsies: their interdependence. 730 59

Hypoglycaemia is a known complication of fulminant hepatic failure. Massive destruction of liver tissue, along with hyperinsulinism and defective glucose storage in extrahepatic organs are some of the mechanisms contributing to the hypoglycaemia. We describe here a case of reversal of fulminant-hepatitis-associated hypoglycaemia at the anhepatic stage of liver transplantation. It is suggested that non-insulin hypoglycaemic factors secreted by the damaged liver may be responsible for this complication.
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PMID:Reversal of fulminant-hepatitis-associated hypoglycaemia at the anhepatic stage during liver transplantation. 871 32

Glucocorticoid excess causes insulin resistance i.e. a reduced effectiveness of insulin to suppress hepatic glucose production and to increase glucose uptake in muscle and fat tissue. Persons who cannot compensate for the resulting additional insulin need develop overt diabetes during glucocorticoid therapy. In the field of gastroenterology, glucocorticoids are mainly employed for the therapy of chronic inflammatory bowel diseases, alcoholic and autoimmune hepatitis, and after liver transplantation. The risk of developing steroid diabetes depends among other things on the genetic predisposition, the body composition, the underlying gastrointestinal disease, the age, and the steroid dose. The treatment of glucocorticoid-induced diabetes resembles essentially the treatment of type 2-diabetes. In addition to dietary measures, oral antihypoglycemic drugs and/or insulin are applied. If oral antihypoglycemic drugs are used, specific problems that might result from the gastrointestinal diseases need to be observed. In the short and medium term, the prognosis of glucocorticoid-induced diabetes is good since it is well treatable. If glucocorticoid treatment is continued for a long time, the alterations of glucose metabolism and the resulting hyperinsulinemia may lead to increased cardiovascular risk.
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PMID:[Glucocorticoid-induced diabetes mellitus in gastrointestinal diseases]. 1044 14

The levels of dehydroepiandrosterone (DHEA) and its sulfate (DHEA-S) peak in human in their twenties, then decrease gradually with age. The physiological importance of DHEA was not clear until recent research reports showing that DHEA has beneficial effects on preventing diabetes, malignancy, inflammation, osteoporosis, and collagen disease. We summarize our results concerning diabetes, hepatitis, and colon cancer. In 1982, Coleman et al. [Diabetes 31 (1982) 830] reported that DHEA decreased hyperglycemia in diabetic db/db mice, which become insulin resistant. We measured hepatic gluconeogenic enzymes in an attempt to elucidate the mechanical mechanism of DHEA action. The activity and gene expression of hepatic gluconeogenic enzyme such as glucose-6-phosphatase (G6Pase) was increased in db/db mice despite hyperinsulinemia compared to control db/+m mice. DHEA, like troglitazone, decreased these levels in db/db mice. We also showed that DHEA improved the insulin resistance caused by aging or obesity using the glucose clamp technique in another animal model. In humans, the serum DHEA concentration was shown to be associated with hyperinsulinemia in diabetes. It also became clear that DHEA increased insulin secretion in old-aged db/db mice. DHEA increases not only insulin sensitivity due to the effects in the liver and muscle, but also insulin secretion. As an effect of DHEA on T-cell mediated hepatitis induced by concanavalin A (ConA), DHEA reduced hepatic injury by inhibiting several inflammatory mediators and apoptosis. As an effect of DHEA on carcinogenesis, DHEA would be a potential chemopreventative agent against colon cancer because it decreases the number of azoxymethane (AOM) induced aberrant crypt foci, which is a possible precursor to adenoma and cancer in a murine model.Thus, since DHEA has many beneficial effects experimentally, we should consider administration of DHEA in the future, and common mechanisms among these actions of DHEA should be elucidated in further studies.
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PMID:Prevention of diabetes, hepatic injury, and colon cancer with dehydroepiandrosterone. 1294 37

Lipodystrophies are a group of diseases characterized by loss of fat tissue and are associated with insulin resistance. A six-year-old girl followed with the diagnosis of autoimmune hepatitis showed a severe loss of fat tissue, hyperinsulinemia, impaired glucose tolerance, hypertriglyceridemia and low serum complement 4 (C4) levels. She had coarse facial features with generalized loss of subcutaneous fat and prominent muscularity. Remarkable acanthosis nigricans was present over the neck, axilla, and umbilicus. Two hours after glucose loading, the glucose tolerance test revealed a glucose level of 258 mg/dL, a HbA1c value of 6.8%, and an insulin level of 642.9 mIU/mL, documenting a state of insulin resistance and type 2 diabetes mellitus. Acquired generalized lipodystrophy was diagnosed and metformin with dietary intervention was initiated. Low serum complement levels proved the autoimmune nature of the process. We conclude that the serum complement levels must be investigated in patients with acquired lipodystrophy, particularly when it is associated with autoimmune hepatitis.
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PMID:Acquired generalized lipodystrophy associated with autoimmune hepatitis and low serum C4 level. 2127 35


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