Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work in our laboratory and others suggests that protein malnutrition plays an important role in the pathogenesis of hepatic steatosis and dysfunction which characteristically appears after jejunoileal bypass for morbid obesity. Postoperative protein-calorie malnutrition is at least in part a consequence of diminished intestinal absorption of free amino acids. In an attempt to prevent liver disease, six morbidly obese patients were orally supplemented with essential amino acids for 4 months after surgery. Oral amino acid supplementation only partially influenced protein malnutrition and had no effect on deterioration of hepatic morphology and dysfunction. Although this mode of therapy appears to be ineffective in preventing postoperative liver abnormalities, other studies suggest that oral oligopeptide supplementation and parenteral administration of amino acids are beneficial. In addition to protein deificiency, other factors which may contribute to the development of liver disease are reviewed.
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PMID:Effect of oral amino acid supplementation on liver disease after jejunoileal bypass for morbid obesity. 40 55

Fatty infiltration of liver and formation of cholesterol stones are significant problems following jejunoileal bypass for morbid obesity. This report evaluates hepatic lipid metabolism and fat absorption in genetically obese, bypassed, and lean Zucker rats. Ninety percent jejunoileal bypass was performed in 12 (500 grams) obese rats (BP). Similar numbers of unoperated "fat rats" (FR) and lean litter mates (LR) were controls. Food consumption, weight gain or loss, and fecal fat were evaluated. At 4 weeks serum triglycerides, hepatic cholesterol, total lipids, triglycerides, and hepatic synthesis of fatty acids and cholesterol were measured in vivo. Food intake was excessive in FR's (23.8 +/- 0.7 gm/day), decreased in BP (18.3 +/- 2.3 gm/day), and lowest in LRss ( less than 0.05) and excessive fecal fat excretion (p less than 0.05). Serum triglycerides were elevated in FR's (284 +/- 32 mg/dl), reduced in BP rats (148 +/- 20 mg/dl) (p less than 0.05), and low in LR's (86 +/- 16 mg/dl). Total hepatic lipids, triglycerides, and hepatic synthesis of fatty acids were elevated in FR's (p less than 0.05) and were unchanged by bypass. Hepatic cholesterol was similar in all groups. Hepatic synthesis of cholesterol, however, was increased significantly in bypassed rats (p less than 0.05), (BP--102 +/- 22 micronnmole/"C2"/minute/gm, FR--39 +/- 6.0, LR--30 +/- 4.0). Jejunolileal bypass in FR's results in weight loss, decreased food intake, increased fecal fat, decreased serum triglycerides, and increased hepatic synthesis of cholesterol. Bypass had little effect on reducing elevated hepatic lipids, triglycerides, or fatty acid synthesis in FR's. These data suggest that following bypass increased hepatic cholesterol synthesis (as a precursor for bile acids) is related to interruption of the enterohepatic circulation and bile salt pool depletion. This implies that excess synthesis of hepatic cholesterol results in supersaturation of bile which is choletithocenic and may explein in part the increased incidence of gall stones observed following jejunoileal bypass.
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PMID:Increased hepatic synthesis of cholesterol following jejunoileal bypass. 87 Oct 14

1. Childhood obesity has been increasing for the last ten years in Tateyama City. Obesity in boys between the ages of 11 to 13 years was especially prominent. 2. Childhood obesity hardly improved especially in middle and morbid obesity. Eighty-five percent of light obesity in children lead to adult obesity. 3. Complications such as hypertension, serum lipid disorder and fatty liver were also observed in childhood obesity. Considering that Tateyama City is a typical Japanese country city, the above results could be representative of Japanese childhood obesity. Recent increases in childhood obesity might be due to the westernized dietary habit.
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PMID:Incidence of childhood obesity over the last 10 years in Japan. 228 54

Hepatocytes and bile duct epithelium express several types of cytokeratins, the characteristic intermediate-filament proteins of epithelial cells. The cytokeratin antigen expression was studied in normal and diseased livers, intrahepatic cholangiocarcinomas, and hepatocellular carcinomas by immunohistochemical methods using a panel of polyclonal and monoclonal antibodies to cytokeratins. Ten percent formaldehyde solution-fixed, paraffin-embedded sections obtained from ten patients without liver disease, 18 patients without liver disease, 18 patients with different stages of primary biliary cirrhosis, 14 patients with alcoholic hepatitis, ten patients with fatty liver hepatitis secondary to diabetes mellitus or morbid obesity, five patients with hepatocellular carcinomas, and five patients with cholangiocarcinomas were examined. The results suggested that hepatocytes and bile duct epithelium retain their distinct cytokeratin profiles in liver disease, including malignant transformation. Therefore, demonstration of cytokeratins in the liver is useful in establishing the cellular origin of neoplasms and understanding the pathogenesis of liver diseases.
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PMID:Expression of cytokeratins in normal and diseased livers and in primary liver carcinomas. 246 75

Small intestinal bypass performed for morbid obesity produces hepatic fat infiltration which persists in some patients for more than 5 years. In an attempt to define causative and preventative factors of hepatic steatosis following small intestinal bypass, a rat model was developed. In this study, nutritionally obese rats underwent sham operations or bypass of 90 per cent of their small intestine and postoperatively were fed various diets to determine the effects of dietary manipulations on hepatic lipid content. After 30 days the rats were killed and their hepatic lipid content and lipogenic enzyme activity determined. In rats that underwent intestinal bypass neither a high fat, a high carbohydrate nor a high protein diet increased hepatic lipid content over that present in sham operated animals. A low (4.5 per cent) protein diet increased total hepatic lipid and hepatic triglyceride content. The increased triglyceride levels were not associated with significant changes in lipogenic enzyme activity and were associated with decreased serum triglycerides suggesting impaired triglyceride transport from the liver secondary to decreased lipoprotein formation as a possible etiologic mechanism. A significant inverse relationship was found between hepatic triglyceride content and hepatic protein content. These results support previous reports from human studies of hypoproteinemia associated with hepatic steatosis following small intestinal bypass.
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PMID:The effect of dietary manipulation on hepatic lipid accumulation in rats undergoing small intestinal bypass. 286 26

The influence of moderate obesity on the liver was assessed in 4613 male company employees including 534 moderately obese subjects (30-50 percent overweight). Serum levels of transaminases and gammaglutamyl transferase activities were significantly higher in moderately obese male non-drinkers than in non-obese non-drinkers. Twenty-four percent of male non-drinkers with moderate obesity had abnormal levels of sGPT and 47 percent of moderately obese male non-drinkers had significant hepatic steatosis as assessed by computed tomography. Although most previous studies on this subject were concerned with morbid obesity accompanying only those of more than 50 percent overweight or those who required surgery, the results of this study clearly indicate that moderately obese subjects also have frequent liver dysfunction.
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PMID:Liver function in moderate obesity--study in 534 moderately obese subjects among 4613 male company employees. 287 56

The prevalence of fatty liver disease at autopsy ranges from 40% to 80% in Europe and North America, and liver injury tests are abnormal in up to 8% of healthy populations. Liver injury tests were therefore examined in a group of 325 workers without exposure to hepatotoxins to identify the influence of obesity and gender. Obesity was a strong predictor of the degree of abnormality for serum levels of arginine and alanine aminotransferase and of alkaline phosphatase, even in the normal range. Women generally demonstrated lower levels of these enzymes. Workers with morbid obesity were substantially more likely to have abnormal liver injury tests. Obesity and gender must be considered in the interpretation of abnormal liver injury tests in hazardous waste workers.
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PMID:Liver injury tests in hazardous waste workers: the role of obesity. 291 8

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
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PMID:Fatty liver disease in morbid obesity. 331 4

A patient died after gastric surgery for morbid obesity. Necropsy showed severe fatty liver, and biochemical analysis of hepatic lipids showed unusually high free fatty acid concentrations, which may have contributed to the hepatic failure.
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PMID:Raised hepatic free fatty acids in a patient with acute fatty liver after gastric surgery for morbid obesity. 372 18

Morbid obesity has been associated with hepatic steatosis and occasional cirrhosis. Despite producing weight loss, intestinal bypass procedures formerly performed to correct morbid obesity, often worsened steatosis and fibrosis, and occasionally resulted in hepatic failure. Current surgical procedures of choice for morbid obesity involve gastric bypass with gastrojejunostomy. Ninety-one liver biopsies taken at the time of gastric bypass for morbid obesity (mean body weight 125.8 kg), and 106 biopsies taken from the same patients from 2 to 61 months later (mean body weight 89.4 kg) were studied. Steatosis and perisinusoidal fibrosis were assessed in histologic sections. Serum albumin, alkaline phosphatase, aspartate aminotransferase (AST), and total bilirubin levels were measured before most biopsies were taken. Both pre- and post-gastric bypass hepatic steatosis varied directly with body weight (r = .5231, P < .001). Steatosis varied inversely with length of time after gastric bypass (r = .4590, P < .001). Of the original biopsies, 37% had lipid vacuoles in at least 26% of hepatocytes. After gastric bypass, 65 patients had reduced steatosis, 18 patients with no steatosis, and 5 patients with minimal steatosis had no change, and 3 patients had increased steatosis. Pre-gastric bypass biopsies from 13 patients had perisinusoidal fibrosis (PSF) that was marked with bridging in three patients, was moderate in one patient, and slight in nine patients. Following gastric bypass, PSF was eliminated in 10 patients, reduced in one patient, and the same in two patients. One patient developed PSF after gastric bypass. Of the three patients who had undergone previous intestinal bypass procedures, two had slight PSF in the biopsies taken at the time of gastric bypass, and one of these had slight PSF in the follow-up biopsy. Serum biochemical abnormalities tended to be slight. Before gastric bypass, serum albumin was low in 11% of cases, alkaline phosphatase was high in 14% of cases, AST was high in 11% of cases, and total bilirubin was high in 1% of cases. After gastric bypass, there was a small reduction in mean serum albumin from 43 g/L before to 41 g/L afterward (P < .05), and a slight rise in mean total bilirubin from 7.0 mumol/L before to 9.6 mu mol/L afterward (P < .01). Most hepatic fatty change and probably some PSF occurring in morbidly obese persons is reduced or eliminated with weight loss following gastric bypass surgery.
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PMID:Regression of hepatic steatosis in morbidly obese persons after gastric bypass. 761 Nov 76


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