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

Fish oil treatment was used in reversing the morphological and metabolic changes of C57BL/6 mice fed high-fat-high-sucrose (HFHS) diet. Two-month-old male C57BL/6 mice were fed HFHS chow or standard chow (SC). At 3 months of age, HFHS mice were separated into an untreated group (HFHS) and a group treated with fish oil (HFHS-Fo, 1.5g/kg/day). At 4 months of age, HFHS fed mice had an increase in body mass (BM) and total body fat, when the animals were sacrificed. Both parameters were lower in HFHS-Fo than in HFHS mice. Plasma glucose and insulin levels were not affected among the groups, but HFHS and HFHS-Fo animals had higher homeostasis model assessment for insulin resistance HOMA-IR ratio. HFHS and HFHS-FO mice had increased plasma total cholesterol and LDL-C, HFHS-Fo increased plasma HDL-C and decreased triglycerides levels. The liver mass (LM) and the adipocytes' size were larger in HFHS mice, while HFHS-Fo mice had a lower LM and smaller adipocytes. The liver steatosis and hepatocyte binucleation were increased in HFHS mice, while HFHS-Fo mice had reduced liver steatosis and hepatocyte binucleation. HFHS-Fo mice had a lower pancreas mass, while HFHS animals had higher islet pancreatic diameter. The SC group showed strong expression for insulin, glucagon and a glucose transporter type 2 GLUT-2 in all pancreatic islets, while in HFHS mice there was less expression for GLUT-2. However, HFHS-Fo mice showed an increase of GLUT-2 expression. In conclusion, dietary fish oil treatment reduces body mass and fat pad adiposity, and also by reducing plasma TG and pancreatic islet hypertrophy in mice fed high-fat-high-sucrose diet. Furthermore, fish oil improves glucagon and GLUT-2 expressions when it is decreased in insulin, but in hepatocyte binucleation and hepatic steatosis where the effect is reduced.
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PMID:Adipose tissue, liver and pancreas structural alterations in C57BL/6 mice fed high-fat-high-sucrose diet supplemented with fish oil (n-3 fatty acid rich oil). 1918 42

The prevalence of metabolic syndrome has been increased recently because of westernized dietary habits and low physical activity in Japan. Metabolic syndrome is diagnosed by the accumulation of dislipidemia, glucose intolerance and/or high blood pressure caused by visceral obesity. The dislipidemia in metabolic syndrome is characterized by the presence of high plasma triglyceride and low HDL-cholesterol, which are associated with increase in small dense LDL and remnant lipoproteins, highly atherogenic lipoproteins. Metabolic syndrome is also often associated with fatty liver, which may be led to non-alcoholic steatohepatitis (NASH). Reduction of body weight and increase in physical activities are highly recommended in overweight patients to inhibit the development of metabolic syndrome, the dislipidemia and NASH.
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PMID:[Dislipidemia and steatohepatitis with visceral fat]. 1920 10

Lysosomal acid lipase (LAL) deficiency results in Wolman disease and cholesteryl ester storage disease (CESD), a more benign form. CESD is a recessive disorder characterized by hypercholesterolaemia, hypertriglyceridaemia, low blood HDL and variable phenotype, while hepatomegaly is usually evident during childhood or adolescence. An 11-year-old girl was referred to our department for combined hyperlipidaemia (total cholesterol 323, triglycerides 259 mg/dl). All family members had normal lipid profile and liver function tests. At 8 years she was admitted for acute Epstein-Barr virus infection, with hepatosplenomegaly and elevation of liver enzymes. Liver-spleen enlargement resolved, but serum alanine aminotransferase and aspartate aminotransferase were persistently twice the upper limits, with other liver function tests within the normal range. Ultrasonography showed normal liver and spleen size and minimal hepatic steatosis. Infectious, autoimmune and metabolic causes of elevated liver enzymes were ruled out, including glycogen storage disease. Dysbetalipoproteinaemia was also ruled out (ApoE phenotype: E3E3). In the following 2 years the girl was symptom-free, BMI was at the 50th-75th centile for age and lipid profile was unchanged despite a low-fat diet. At 13 years of age, low acid lipase activity was demonstrated in leukocytes (10 nmol/h/ per mg protein, normal 140-380) and cultured skin fibroblasts (181 nmol/h per mg protein, normal 1100-2400), leading to diagnosis of CESD. CESD usually progresses to hepatic fibrosis, with high risk of premature atherosclerosis. CESD prevalence may be underestimated in the general population. The diagnosis may be considered in all subjects with atypical combined hyperlipidaemia (usually dominant in transmission or related to metabolic syndrome) and atypical 'fatty liver disease', in the absence of overweight.
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PMID:Combined hyperlipidaemia as a presenting sign of cholesteryl ester storage disease. 1921 73

Insulin resistance may favor increased urinary albumin excretion (UAE), leading progressively to chronic kidney disease (CKD). A recent study on non-alcoholic fatty liver disease (NAFLD), a condition of insulin resistance, associated this disease with the incidence of CKD in patients with type 2 diabetes. The aim of our study was to determine whether there is an association between insulin resistance and kidney function, based on estimates of UAE and creatinine clearance in children with biopsy-proven NAFLD. Kidney function was assessed in 80 patients with NAFLD and 59 individuals of normal weight matched for age and sex. Insulin resistance was measured by means of the homeostatic model assessment-insulin resistance (HOMA-IR) and limited to NAFLD patients by using the whole-body insulin sensitivity index. The HOMA-IR was found to differ significantly between the two groups (2.69 +/- 1.7 vs. 1.05 +/- 0.45; p = 0.002), while UAE (9.02 +/- 5.8 vs. 8.0 +/- 4.3 mg/24 h; p = 0.9) and creatinine clearance (78 +/- 24 vs. 80 +/- 29 mg/min; p = 0.8) did not. We found a significant but weak inverse correlation between insulin sensitivity and creatinine clearance in NAFLD patients (r (s) = -0.25;p = 0.02). No difference was observed in kidney function between NAFLD children presenting with or without metabolic syndrome, low or normal HDL-cholesterol, and different degrees of histological liver damage (grade of steatosis >or=2, necro-inflammation, and fibrosis). Patients with hypertension had increased levels of UAE (p = 0.04). A longer exposure to insulin resistance may be required to cause the increase in urinary albumin excretion and to enable the detection of the effect of the accelerated atherogenic process most likely occurring in children with fatty liver disease. Longitudinal studies are needed to rule out any causative relationship between insulin resistance and urinary albumin excretion.
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PMID:Albuminuria and insulin resistance in children with biopsy proven non-alcoholic fatty liver disease. 1924 28

Young adults with abdominal obesity are liable to have subclinical atherosclerosis that may contribute to an increased risk of cardiovascular disease later in life. This study aims to evaluate subclinical atherosclerosis and its possible correlation with some inflammatory and biochemical markers in Egyptian young adult males with abdominal obesity. The study includes 50 young adult males (age range: 19-29 years) divided into two groups. Group 1 comprises 20 non-obese subjects (controls). Group 2 comprises 30 apparently healthy obese subjects. Carotid intima media thickness (carotid-IMT) was estimated using B-mode ultrasonography of the common carotid arteries, and abdominal ultrasonography was performed to assess the presence of a fatty liver. Laboratory investigations included fasting levels of serum glucose, triglycerides (TG), cholesterol (total [TC], high-density [HDL-cholesterol] and low-density [LDL-cholesterol] lipoprotein fractions), high-sensitivity C-reactive protein (hs-CRP), neopterin, lipoprotein-a (Lp[a]), gamma glutamyl transferase (GGT), aspartate and alanine aminotransferases (AST, ALT), plasma plasminogen and fibrinogen. Results showed that carotid IMT, serum hs-CRP, neopterin, Lp(a), fibrinogen, plasminogen, TC, TG, LDL-cholesterol and liver enzymes were significantly elevated (P<0.001) in the obese group compared to controls. All obese subjects showed evidence of fatty liver. A significant positive correlation was found between carotid-IMT and body mass index, waist circumference, waist/hip ratio, cholesterol, triglycerides, neopterin, hs-CRP AST, ALT and GGT. Elevated serum levels of inflammatory biomarkers and increased ALT, AST and GGT, and non-alcoholic fatty liver disease biomarkers may be useful predictors of subclinical atherosclerosis.
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PMID:Evaluation of some markers of subclinical atherosclerosis in Egyptian young adult males with abdominal obesity. 1983 25

Prague hereditary hypercholesterolemic (PHHC) rat - rat strain crossbred from Wistar rats - is a model of hypercholesterolemia induced by dietary cholesterol. Importantly, no bile salts and/or antithyroid drugs need to be added to the diet together with cholesterol to induce hypercholesterolemia. PHHC rats have only modestly increased cholesterolemia when fed a standard chow and develop hypercholesterolemia exceeding 5 mmol/l on 2 % cholesterol diet. Most of the cholesterol in hypercholesterolemic PHHC rats is found in VLDL that become enriched with cholesterol (VLDL-C/VLDL-TG ratio > 1.0). Concurrently, both IDL and LDL concentrations rise without any increase in HDL. PHHC rats do not markedly differ from Wistar rats in the activities of enzymes involved in intravascular remodelation of lipoproteins (lipoprotein and hepatic lipases and lecithin:cholesterol acyltransferase), LDL catabolism, cholesterol turnover rate and absorption of dietary cholesterol. The feeding rats with cholesterol diet results in development of fatty liver in spite of suppression of cholesterol synthesis. However, even though cholesterolemia in PHHC rats is comparable to human hypercholesterolemia, the PHHC rats do not develop atherosclerosis even after 6 months on 2 % cholesterol diet. Importantly, the crossbreeding experiments documented that hypercholesterolemia of PHHC rats is polygenic. To identify the genes that may be involved in pathogenesis of hypercholesterolemia in this strain, the studies of microarray gene expression in the liver of PHHC rats are currently in progress.
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PMID:Prague hereditary hypercholesterolemic (PHHC) rat - a model of polygenic hypercholesterolemia. 2013 41

The effects of taurine on plasma and liver cholesterol, erythrocyte ouabain sensitive Na efflux and platelet aggregation were examined in Sprague Dawley rats fed control or 0.5% cholesterol with 0.2% cholate diet. Plasma and liver levels of total cholesterol were increased significantly (p<0.05) in rats fed cholesterol diet compared to the control, and taurine significantly decreased the elevated plasma level of cholesterol in rats fed cholesterol diet (p<0.05). HDL-cholesterol was decreased in groups fed the cholesterol diet regardless of taurine supplementation and the difference between groups with and without cholesterol was significant (p<0.01). Plasma triglyceride was decreased and liver triglyceride was increased both significantly (p<0.05) in rats fed cholesterol compared to the control. Plasma and liver triglyceride in rats fed taurine was decreased significantly compared to the control (p<0.05). Intracellular Na tended to be lower in rats fed cholesterol or taurine and higher in rats fed cholesterol plus taurine compared to the control. Na efflux through Na-K ATPase and the passive leak of Na was somewhat reduced in rats fed cholesterol or taurine and was augmented in rats fed cholesterol plus taurine compared to the control, which showed a similar trend to the intracellular Na. Taurine supplementation caused a suppression of Na efflux in groups fed control diet and restored the suppressed Na efflux in groups fed cholesterol. Platelet aggregation was significantly decreased in the group fed taurine compared to the control (p<0.05) and the group fed cholesterol plus taurine was also a little lower in aggregation than the group fed cholesterol. Microscopic examination showed that taurine prevented fatty liver in rats fed cholesterol diet. Taurine known for stimulating Na-K ATPase in some cell types rather decreased erythrocyte ouabain sensitive Na-K ATPase in the present study. Taurine had hypolipidemic and hypocholesterolemic effects and inhibited platelet aggregation which may be favorable for prevention of cardiovascular diseases.
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PMID:Effects of taurine on plasma and liver lipids, erythrocyte ouabain sensitive Na efflux and platelet aggregation in Sprague Dawley rats. 2036 39

Incidence of obesity and hepatic steatosis is increasing worldwide. Almost one quarter of western countries population suffer from non alcoholic fatty liver disease (NAFLD). The aim of this study was to investigate the frequency and predictors of nonalcoholic steatohepatitis (NASH) in patients with unexplained alanine aminotransferase activity elevation (ALT), and therefore avoid unnecessary biopsies in cases of simple steatosis. Earlier studies provided different results and have not answered the question how to distinguish NASH from simple steatosis. Ultrasound (US), computed tomography (CT) and magnetic resonance (MRI) can detect steatosis with great sensitivity level, but not NASH. This study included 50 patients (18 women and 32 men) with mean age 43 +/- 9 years, and with defined selected biochemical, anthropometric and hormone biomarkers. The average BMI was 27.1 +/- 3.81 (kg/m2), insulin resistance HOMA IR 3.89 +/-3.81. All patients underwent liver biopsy and NASH was staged by NASH activity score (NAS) from 1 to 8. Results are compared to pathohistological finding as relevant method. The results show that 90% of patients (n=45) had NAFLD (minimal stage at least), and 15 (30%) had nonalcoholic steatohepatitis (NASH). High triglyceride, low HDL and high ferritin serum levels correspond with NASH. As in earlier studies, insulin resistance as basic mechanism of NAFLD and NASH was confirmed.
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PMID:Predictors of nonalcoholic steatohepatitis in patients with elevated alanine aminotransferase activity. 2040 93

Dietary sphingolipids (SL) inhibit colon carcinogenesis, reduce serum cholesterol, and improve skin barrier function and are considered to be "functional lipids". For comparative determination of the effects of SL with different chemical compositions on lipid metabolism and its related hepatic gene expression, Zucker fatty rats were fed pure sphingomyelin (SM) of animal origin and glucosylceramide (GC) of plant origin. After 45 days, the SM and GC diets led to significant reductions in hepatic lipid and plasma non-HDL cholesterol. Both SM and GC diets decreased plasma insulin levels, whereas only the GC diet increased the plasma adiponectin level. Hepatic gene expression analysis revealed increased expression of adiponectin receptor 2 (Adipor2), peroxisome proliferator-activated receptor alpha (PPARalpha), and pyruvate dehydrogenase kinase 4 (Pdk4). However, expression of stearoyl CoA desaturase (Scd1) was significantly decreased. These results suggest that dietary SL, even of different origins and chemical compositions, may prevent fatty liver and hypercholesterolemia through improvement of adiponectin signaling and consequent increases in insulin sensitivity.
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PMID:Dietary sphingolipids ameliorate disorders of lipid metabolism in Zucker fatty rats. 2044 4

Recently detected 152 IGT and 158 type 2 diabetes patients aged between 30 and 69 years, never treated with any antidiabetic drug, lipid lowering agent, angiotension converting enzyme (ACE) inhibitor and/or angiotensin receptor blocker (ARB) were evaluated. One hundred and sixty asymptomatic, willing, healthy, normoglycaemic spouse or unrelated attendants accompanying the patients were also selected. History of significant alcohol intake or hepatotoxic drugs and positive serologic findings for hepatitis B and C viruses were excluded. The prevalence of fatty liver was 64% in type 2 DM, 52% in impaired glucose tolerance (IGT) and 20% in normal glucose tolerance (NGT) subjects. Subjects with fatty liver had significantly higher body mass index (BMI), waist, waist hip ratio, waist to height ratio, triglyceride, fasting insulin, insulin resistance (HOMA-IR), along with significantly lower HDL-C and quantitative insulin-sensitivity check index (QUICKI) compared to those without fatty liver. Similar findings were noted in subjects with fatty liver in the subgroups of NGT, IGT and diabetes as well, for the above mentioned parameters. There was no significant difference in total cholesterol, LDL-C between subjects with or without fatty liver. However, analysis by the multivariate regression technique revealed that QUICKI (but not HOMA-IR), waist circumference and waist to height ratio had a significant association (p < 0.01 for all groups and for all these three parameters except in the NGT group for waist to height ratio p < 0.05) with development of fatty liver. BMI on the other hand was not significantly associated with the fatty liver in the multivariate regression (p = 0.067).
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PMID:Central obesity but not generalised obesity (body mass index) predicts high prevalence of fatty liver (NRFLD), in recently detected untreated, IGT and type 2 diabetes Indian subjects. 2046 78


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