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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

During embryonic development, insulin-like growth factor-II (IGF-II) participates in the regulation of islet growth and differentiation. We generated transgenic mice (C57BL6/SJL) expressing IGF-II in beta cells under control of the rat Insulin I promoter in order to study the role of islet hyperplasia and hyperinsulinemia in the development of type 2 diabetes. In contrast to islets from control mice, islets from transgenic mice displayed high levels of IGF-II mRNA and protein. Pancreases from transgenic mice showed an increase in beta-cell mass (about 3-fold) and in insulin mRNA levels. However, the organization of cells within transgenic islets was disrupted, with glucagon-producing cells randomly distributed throughout the core. We also observed enhanced glucose-stimulated insulin secretion and glucose utilization in islets from transgenic mice. These mice displayed hyperinsulinemia, mild hyperglycemia, and altered glucose and insulin tolerance tests, and about 30% of these animals developed overt diabetes when fed a high-fat diet. Furthermore, transgenic mice obtained from the N1 backcross to C57KsJ mice showed high islet hyperplasia and insulin resistance, but they also developed fatty liver and obesity. These results indicate that local overexpression of IGF-II in islets might lead to type 2 diabetes and that islet hyperplasia and hypersecretion of insulin might occur early in the pathogenesis of this disease.
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PMID:Transgenic mice overexpressing insulin-like growth factor-II in beta cells develop type 2 diabetes. 1072 41

One hundred and twenty-seven consecutive morbidly obese patients who presented for bariatric surgery underwent open wedge liver biopsy at the completion of their gastric restrictive procedure. All hepatic specimens were graded histologically for degrees of steatosis. Three-quarters of the patients had histological evidence of hepatic steatosis and in one-fifth this was severe and diffuse. No patient had histological evidence of fatty hepatitis, portal fibrosis, or cirrhosis. There was no significant correlation between the degree of obesity (measured as percentage over ideal weight), age, sex, or preoperative liver function tests and the degree of fatty change observed. Insufficient data were available to Implicate alcohol and poor protein nutrition in the etiology of the observed fatty liver change. Other factors such as diabetes mellitus or drugs were not etiologic factors in this series of patients.
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PMID:Hepatic Steatosis and Morbid Obesity. 1075 12

Hepatic morphology and clinical course of mildly obese subjects with abnormal liver tests were determined in comparison with those of surgically treated morbidly obese cases. Twenty mildly obese subjects (mean body mass index, 27.9) with elevated serum transaminase levels were followed up on a low-calorie diet. Nineteen morbidly obese patients (mean body mass index, 39.2) had a surgical biopsy at gastric restrictive surgery. In these two groups, the frequency and the severity of hepatic steatosis and fibrosis were comparable, whereas intralobular cell infiltration was somewhat greater in the mildly obese group. Follow-up studies of the two groups showed remarkable improvement of serum transaminase levels, the extent of which was greater in surgically treated cases. Thus, in mildly obese subjects with abnormal liver tests, (1) hepatic histological abnormalities are not milder than those in morbidly obese cases, and (2) Improvement of serum transaminase levels upon diet therapy is less satisfactory than that in morbidly obese cases treated surgically. It is suggested these two groups may not be in the same spectrum of obesity-related hepatic disorders.
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PMID:Hepatic Abnormalities in Obesity: comparison between mildly obese cases and morbidly obese cases. 1076 62

Nonalcoholic steatohepatitis (NASH) is a histological diagnosis applied to a constellation of liver biopsy findings that develop in the absence of alcohol abuse. Steatosis, a mixed cellular inflammatory infiltrate across the lobule, evidence of hepatocyte injury and fibrosis are the findings that can be seen. This entity is often identified during evaluation of elevated aminotransferases after exclusion of viral, metabolic and other causes of liver disease. Obesity is a major risk factor for NASH. The role of diabetes is less certain, although evidence is accumulating that hyperinsulinism may play an important pathophysiological role. Patients sometimes suffer from right upper quadrant abdominal pain and fatigue; examination may reveal centripetal obesity and hepatomegaly. Although patients are often discovered because of persistent aminotransferase elevations, these enzymes can be normal in NASH. When they are elevated, the alanine aminotransferase level is typically significantly greater than the aspartate aminotransferase level. This can be particularly helpful for excluding occult alcohol abuse. Imaging studies identify hepatic steatosis when the amount of fat in the liver is significant; however, imaging does not distinguish benign steatosis from NASH. Ultimately a liver biopsy is needed to diagnose NASH. The biopsy may be useful for establishing prognosis based on the presence or absence of fibrosis and for excluding other unexpected causes of liver enzyme elevations. Weight loss is the mainstay of treatment for obese patients. About 15% to 40% of NASH patients develop fibrosis; how many of these cases progress to cirrhosis is unknown, but about 1% of liver transplants are performed with a pretransplant diagnosis of NASH.
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PMID:Nonalcoholic steatohepatitis: an evolving diagnosis. 1079 85

An aqueous extract of Platycodi radix inhibited the hydrolysis of triolein emulsified with phosphatidylcholine by pancreatic lipase in vitro and it reduced the elevation of rat plasma triacylglycerol level 2-4 h after oral administration of a lipid emulsion containing corn oil. These preliminary results suggested that the aqueous extract of Platycodi radix may inhibit the intestinal absorption of dietary fat by inhibiting its hydrolysis. Therefore, we examined the antiobesity activity of the aqueous extract of Platycodi radix by testing whether the extract prevented the obesity induced by feeding a high fat diet to mice for 8 wk. Body weights at 3-8 wk and the final parametrial adipose tissue weights were significantly lower in mice fed the high fat diet containing 5% aqueous extract of Platycodi radix than in the controls fed the high fat diet. The aqueous extract of Platycodi radix also significantly reduced hepatic triacylglycerol concentrations that were elevated in mice fed the high fat diet alone. Inulin, which is a major component of Platycodi radix, had no effect on the hydrolysis of triolein emulsified with phosphatidylcholine by pancreatic lipase in vitro, and did not prevent obesity or the fatty liver induced by the high fat diet. On the other hand, the total saponin fraction of the aqueous extract inhibited pancreatic lipase activity in vitro. Therefore, the antiobesity effect of the aqueous extract of Platycodi radix in mice fed a high fat diet may be due in part to the inhibition of intestinal absorption of dietary fat by the saponins of Platycodi radix.
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PMID:Platycodi radix affects lipid metabolism in mice with high fat diet-induced obesity. 1105 18

Hyperlipidemia is a known risk factor for fatty infiltration of the liver, a condition that can progress to cirrhosis and liver failure. The objectives of this study were to document the prevalence of fatty infiltration in the livers of hyperlipidemic patients and to identify the predictor variables associated with this condition. Over an 18-month recruitment period, clinical, biochemical, and radiologic assessments were performed in a cross-sectional manner in 95 adult patients referred to an urban hospital-based lipid clinic for evaluation and management of hyperlipidemia. The mean (+/-SD) age of the patients was 55 +/- 13 years. Forty-eight (51%) were male. Fifty-two patients (55%) had hypercholesterolemia, 25 (26%) severe hypertriglyceridemia, 14 (15%) mixed hyperlipidemia, and 4 (4%) moderate hypertriglyceridemia. Obesity and diabetes were present in 36 (38%) and 12 (12%) of cases, respectively. A total of 61 (64%) patients had elevated liver enzyme tests. The most common enzyme abnormalities were an elevated serum ALT in 45 (47%) and GGT in 43 (45%) of patients. Ultrasound findings revealed diffuse fatty liver in 47 patients (50%), of which 21 cases (22%) were mild, 18 (19%) moderate, and 8 (9%) severe. The majority of patients with hypercholesterolemia [35/52 (67%)] had normal ultrasounds, whereas severe hypertriglyceridemia and mixed hyperlipidemia were frequently associated with radiologic evidence of fatty liver (odds ratios 5.9 and 5.1 respectively, P < 0.01). Independent predictors of fatty liver were; AST (P = 0.001), hyperglycemia (P = 0.02), and age (P = 0.04). In a model incorporating known risk factors for fatty liver, diabetes was the only risk factor other than hypertriglyceridemia that was significantly associated with fatty infiltration. No such effect was seen with age, gender, obesity, or alcohol consumption. In conclusions, the results of this study indicate that ultrasonographic evidence of fatty infiltration of the liver is evident in approximately 50% of patients with hyperlipidemia. Hypertriglyceridemia is the lipid profile most often associated with this condition. Serum AST values, hyperglycemia, and age independently predict the presence of fatty infiltration, while hypertriglyceridemia and diabetes are the only risk factors that significantly increase the risk of fatty infiltration in hyperlipidemic patients.
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PMID:Fatty infiltration of liver in hyperlipidemic patients. 1111 62

The rising prevalence of obesity is accompanied by an increasing number of patients with the metabolic complications of obesity. The major complications come under the heading of the metabolic syndrome. This syndrome is characterized by plasma lipid disorders (atherogenic dyslipidemia), raised blood pressure, elevated plasma glucose, and a prothrombotic state. The clinical consequences of the metabolic syndrome are coronary heart disease and stroke, type 2 diabetes and its complications, fatty liver, cholesterol gallstones, and possibly some forms of cancer. At the heart of the metabolic syndrome is insulin resistance, which represents a generalized derangement in metabolic processes. Obesity is the predominant factor leading to insulin resistance, although other factors play a role. The mechanistic link between insulin resistance and the metabolic syndrome is complex. The relationship is modulated by yet other factors, such as physical activity, body fat distribution, hormones, and a person's genetic polymorphic architecture. A better understanding of the molecular basis of this relationship is needed to suggest new targets for prevention and treatment of the complications of obesity. In addition, understanding at the clinical level will lead to improved management of these complications.
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PMID:Metabolic complications of obesity. 1118 17

The report is devoted to the presentation of aetiological factors causing fatty liver, including alcohol, obesity, diabetes mellitus, hyperlipoproteinaemias and drugs. The author discusses morphological changes typical for the fatty liver such as large or small fatty droplets in hepatocytes and rarely coexisting hepatitis (so-called steatohepatitis). The work presents symptoms, changes in biochemical analyses of serum as well as methods of the liver visualisation used in the diagnostics of fatty liver. The treatment in based on the elimination of aetiological factors and properly balanced diet with support of pharmacotherapy in selected cases.
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PMID:Fatty liver--current look at the old disease. 1120 12

Corn oil is well tolerated by mice but tolerance may decrease with excessive ingestion. In the present study, we compared the effects of optional ingestion of excessive corn oil with ingestion of water (control) or a 20% sucrose solution in mice. During the entire study, mice consistently ingested 100% corn oil and incrementally ingested 20% sucrose. Food intake in the corn-oil group was approximately constant but that in the sucrose group was slightly decreased. Body-weight gains in the corn-oil group were higher than those in the control and sucrose groups. At the end of the study, hepatic hypertrophy and fatty liver were present, especially in the corn-oil group, and the visceral fat of mice fed corn oil increased significantly compared with the other two groups. These results suggest that mice, when given a choice, will continue to overeat corn oil over the long term, inducing excessive caloric intake and obesity.
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PMID:Long-term optional ingestion of corn oil induces excessive caloric intake and obesity in mice. 1124 Mar 39

Obesity causes many undesirable health disorders such as diabetes mellitus, hyperlipidemia, hypertension and so on. Recently, those life style-affecting diseases is increasing, especially the increment of diabetes mellitus is prominent. In 2000, Japan obesity society issued the new standard of the evaluation of obesity and new diagnostic criteria of obesity as a disease for Japanese. According to this issue, obesity was evaluated by body mass index(BMI). And, 18.5 < BMI < 25 is normal, 25 < BMI < 30 is obese 1, 30 < BMI < 35 is obese 2, 35 < BMI < 40 is obese 3, and 40 < is obese 4. Obesity as a disease is defined by two cases. The first category is composed of two items; one is BMI > 25, and the other is having one disease worsen by obesity, such as diabetes mellitus, hyperlipidemia, hypertension, hyperuricemia, coronary heart disease, cerebral infarction, sleep apnea syndrome, fatty liver, deformative arthritis. The second category is the visceral type of obesity with BMI > 25, which was diagnosed by west size, over 85 cm for men, and over 90 cm for women, and by visceral fat area over 100 cm2 in abdominal CT.
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PMID:[Evaluation of obesity and diagnostic criteria of obesity as a disease for Japanese]. 1126 12


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