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)

Reported herein is a case of focal hepatic steatosis surrounding a metastatic insulinoma in the liver of a 69-year-old woman. The patient complained of losing consciousness after meals, and hypoglycemia and hyperinsulinemia were confirmed. On CT and abdominal angiography a mass, 1 cm in diameter, was seen in the tail of the pancreas. In the early phase of dynamic CT a mass, 5 mm in diameter, was seen in the liver. In the late phase this mass appeared to be 3 cm in diameter. An arterial calcium stimulation/venous sampling test showed insulin levels after calcium injections in the hepatic artery to be extremely high. Thus, the liver tumor was diagnosed as a metastatic insulinoma, and distal pancreatectomy and partial resection of the liver were performed. The pancreatic tumor cells were immunohistochemically positive for insulin. The liver tumor was pale yellow. A white area surrounded the tumor. Histologically, the liver tumor was an insulinoma and the white area was focal fatty change of the liver. High insulin levels are said to inhibit oxidation of free fatty acids into triglycerides, causing free fatty acids to accumulate in hepatocytes. Focal hepatic steatosis caused by the local effects of insulin can present as a focal rim surrounding a metastatic insulinoma.
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PMID:Focal hepatic steatosis surrounding a metastatic insulinoma. 1806 43

Fructose induces metabolic syndrome in rats; but studies have been criticized for using high concentrations of fructose that are not physiologic, for using only pure fructose, and for not controlling for energy intake. We tested the hypothesis that a 40% sucrose diet (containing 20% fructose) might induce features of metabolic syndrome in male breeder rats independent of excess energy intake. Male Sprague-Dawley breeder rats were pair fed 40% sucrose or isocaloric starch diet for 4 months and evaluated for metabolic syndrome and diabetes. In vitro studies were performed in rat insulinoma cells (RIN-m5F) exposed to uric acid, and markers of inflammation were assessed. Rats fed a 40% sucrose diet developed accelerated features of metabolic syndrome with up-regulation of fructose-dependent transporter Glut5 and fructokinase. Fatty liver and low-grade pancreatic inflammation also occurred. Uric acid was found to stimulate inflammatory mediators and oxidative stress in islet cells in vitro. Sucrose, at concentrations ingested by a subset of Americans, can accelerate metabolic syndrome, fatty liver, and type 2 diabetes mellitus in male breeder rats; and the effects are independent of excess energy intake.
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PMID:Sucrose induces fatty liver and pancreatic inflammation in male breeder rats independent of excess energy intake. 2148 72

Nonalcoholic fatty liver disease (NAFLD) is a serious health-related condition all over the world; the number of patients is increasing in Asian countries including Japan. Better understanding of its pathophysiology is required to develop effective therapeutics, as patients may go on to develop non-alcoholic steatohepatitis and hepatocellular carcinomas. While NAFLD is believed to be associated with metabolic risk factors such as obesity, diabetes, and dyslipidemia, its etiology remains largely unknown and the development or co-existence of NAFLD in patients with insulinoma has not been investigated. A 33-year-old male with an insulinoma, who had been hypoglycemic during the previous four years, developed abnormally elevated levels of liver enzymes and histological fatty liver characteristic of NAFLD by the time of admission to our hospital for resection of an insulinoma. His medical records for the previous eight years revealed that his bodyweight had increased gradually from 60 kg to 71 kg for seven years and then acutely increased to 79 kg in the latest one-year period. This sudden increase was thought to be due to the patient's self-described overeating of fruits to forestall hypoglycemia. Fresh fruits are rich in fructose, and the patient's triglycerides, alanine and aspartate transaminases showed an acute increase in the previous one-year period. After resection of the insulinoma, the levels of these parameters all were mostly restored, which suggests that hyperinsulinemia and subsequent hyperphagia played a role in the development of NAFLD in this case. This is the first report of patient with NAFLD and an insulinoma.
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PMID:A case of insulinoma with non-alcoholic fatty liver disease: Roles of hyperphagia and hyperinsulinemia in pathogenesis of the disease. 2621 68

Hepatic steatosis can occur because of nonalcoholic fatty liver disease (NAFLD), alcoholism, chemotherapy, and metabolic, toxic, and infectious causes. Pediatric hepatic steatosis is also becoming more frequent and can have distinctive features. The most common pattern is diffuse form; however, it can present in heterogenous, focal, multinodular, perilesional, perivascular, subcapsular, and lobar forms. Focal steatosis and fat sparing can occur because of the presence of veins of Sappey, pancreaticoduodenal vein, and aberrant right and left gastric veins, which drain into the liver as third inflow. Hypersteatosis and multinodular forms can mimic metastasis in patients with cancer. Perilesional fat can be seen in insulinoma. Recent introduction of proton-density fat fraction enabled easy and reproducible quantification of hepatic fat. Follow up of patients with NAFLD can be performed for the assessment of treatment response using proton-density fat fraction as biomarker. Multiecho gradient-echo techniques also simultaneously calculate T2* maps, which is important to rule out coexisting hepatic iron overload. NAFLD can progress to steatohepatitis (nonalcoholic steatohepatitis), which can result in cirrhosis. Magnetic resonance (MR) elastography and functional evaluation with Gd-EOB-DTPA are becoming important for monitoring this process. Hepatocellular carcinoma can develop in patients with NAFLD, which is usually a large tumor with necrotic center. In the future, fatty acid maps obtained by MR imaging may allow more detailed analysis of steatosis. MR imaging is superior to ultrasonography and computed tomography for comprehensive evaluation of steatosis.
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PMID:Hepatic Steatosis: Etiology, Patterns, and Quantification. 2798 69