The fatty acid composition of the triglycerides in liver and subcutaneous fat in diabetics in dependence on liver fatty degeneration.
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Adipose Tissue↗
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Non-fatal acute fatty liver of pregnancy.
Four patients are described, admitted during a three-year period, who recovered from acute fatty liver of pregnancy; vomiting and jaundice were the main manifestations of the disease; coma and anuria were absent. During the same period, we observed one patient who died of acute fatty liver of pregnancy. This experience suggests that the non-fatal form of the disorder may be much commoner than the fatal form.
Acute Disease↗
Orally administered ginseng extract reduces serum total cholesterol and triglycerides that induce fatty liver in 66% hepatectomized rats.
The effects of ginseng extract (from the root of Panax ginseng) on factors inducing fatty liver were examined in 66% hepatectomized rats. Oral administration of ginseng extract at 125 or 250 mg/kg/day produced statistically significant reductions in total cholesterol and triglyceride concentrations in the blood 3 days after hepatectomy (P<0.05); the total cholesterol response appeared to be dose-related. Administration of ginseng extract at both doses also reduced total cholesterol and triglyceride concentrations in the liver 3 days after hepatectomy. Food intake and serum chemistry parameters indicating liver and kidney function were unchanged after ginseng administration except for the lipid metabolic parameters. These observations suggest that orally administered ginseng extract can suppress the formation of fatty liver after hepatic resection.
Administration, Oral↗
Acute fatty liver of pregnancy: an unusual presentation.
We describe a case of acute fatty liver that developed during the third trimester of pregnancy. Acute fatty liver of pregnancy (AFLP) is a well-documented medical condition and is important due to its implications on maternal and fetal morbidity and mortality. AFLP is managed with supportive care and close surveillance is needed in patients with a previous history of this disease. Long-term sequelae such as brain damage may also occur. This case was unusual because the patient presented due to a co-incident uterine scar rupture and was subsequently diagnosed with AFLP. Although no association between scar rupture and AFLP has been reported in the scientific literature, the association of abdominal scar dehiscence and liver disease has been reported previously.
Adult↗
Degradation of pigeon liver fatty acid synthetase in the absence of exogenous proteinases.
The homogeneity of pigeon liver fatty acid synthetase has been rigorously tested by physicochemical techniques and crossed-rocket immunoelectrophoresis. The enzyme has also been incubated for 1 h at 100 degrees C in 2% sodium dodecyl sulfate and 0.1 M dithiothreitol. The number of protein components on gel electrophoresis and of dansylated amino acids increased as a function of incubation time. Furthermore, the minor proteins observed after gel electrophoresis cross-reacted with antibody raised to the synthetase. Proteolysis was not chemically mediated by the detergent, the reducing agent or the buffer conditions chosen. Several commercially prepared proteins were not degraded by this procedure, and two proteins were recalcitrant to hydrolysis when included in the same incubation mixture as the synthetase. The inclusion of certain microbial proteinase inhibitors decreased the amount of degradation. This demonstrated that hydrolysis of the synthetase is mediated by a specific vertebrate enzyme which retains activity under denaturing conditions at 100 degrees C. Further degradation is also observed after individual treatment of four limited digestion products from the pigeon liver fatty acid synthetase, suggesting the possibility of an inherent proteolytic activity within the complex.
Animals↗
Is weight reduction an effective therapy for nonalcoholic fatty liver? A systematic review.
PURPOSE: To assess the evidence supporting the efficacy of weight reduction for patients with nonalcoholic fatty liver. METHODS: Potentially relevant studies were identified by a computerized search of databases and a manual search of abstracts from scientific meetings. Studies were included if they reported histology, serum aminotransferase levels, or radiological imaging of the liver in obese adult patients who had undergone weight reduction. Weight reduction regimens included diet, exercise, antiobesity medications, gastric bypass, gastroplasty, or any combination of these interventions. Studies involving jejunoileal or small bowel bypass surgery were excluded. RESULTS: We identified 517 potentially relevant studies, of which 15 met the inclusion criteria: one randomized controlled trial (in abstract form), two nonrandomized controlled trials, nine case series, one retrospective review, and two case reports. Three studies included more than 50 patients, whereas nine studies had 25 or fewer patients. Twelve studies used behavioral, dietary, or pharmacologic therapy for weight reduction, and three studies used surgical interventions. Although all 15 studies demonstrated overall improvement in the measurements of liver outcome after weight reduction, more than half did not report histologic results. CONCLUSION: Despite general acceptance that weight reduction is an effective therapy for nonalcoholic fatty liver, this systematic review found little data to support or refute this recommendation.
Diet↗
A double-blind randomized placebo-controlled trial of orlistat for the treatment of nonalcoholic fatty liver disease.
BACKGROUND & AIMS: Few controlled studies have addressed the issue of effective medical treatment for nonalcoholic fatty liver disease (NAFLD). We herein assessed the effect of orlistat in patients with NAFLD. METHODS: We performed a randomized, double-blind, placebo-controlled study on 52 patients with NAFLD diagnosed by ultrasound (US) and confirmed by liver biopsy (40 patients). The patients were randomized to receive either orlistat (120 mg 3 times daily for 6 months) or placebo. All patients participated in an identical behavioral weight loss program. All patients underwent monthly evaluation by abdominal US; liver enzyme levels, lipid profiles, insulin levels, and anthropometric parameters were monitored, and all patients underwent nutritional follow-up evaluation. Twenty-two patients underwent a second liver biopsy examination at the end of the study. RESULTS: Fifty-two patients were recruited and 44 (mean age, 47.7 y; mean body mass index, 33) completed the study. Serum glucose and insulin levels (P<.03) were significantly higher in the orlistat group, which also presented a higher degree of fibrosis. Body mass index was reduced significantly in each group, with a nonsignificant difference between the groups. Serum alanine transaminase (ALT) levels decreased significantly in both groups, with an almost 2-fold reduction in the orlistat group (48% vs 26.4%). There was a statistically significant reversal of fatty liver by US only in the orlistat group (P<.05). CONCLUSIONS: Orlistat improves serum ALT levels and steatosis on US in NAFLD patients, beyond its effect on weight reduction.
Adolescent↗
[Blood rheological study in rats with fatty liver--with special reference to effects of ethyl icosapentate].
A blood rheological study was conducted using Kikuchi's micro-channel method in rats with fatty liver. Effects of eicosapentaenoic acid (EPA) on blood rheology were also evaluated. Male SD rats given normal feed served as the control. One group was given choline-deficient feed for 4 weeks (EPA (-) group), while another group was daily given EPA (1000 mg/kg) for 4 weeks together with choline-deficient feed (EPA (+) group). The micro-channel passage time was determined using 100 microliters of whole blood. The passage time significantly increased in the EPA (-) group compared to the control (p < 0.01). It significantly decreased in the EPA (+) group compared to the EPA (-) group (p < 0.01). Findings obtained in the present study suggested that blood rheological factors are related to the development of fatty liver and that EPA inhibits fatty changes of the liver by improving these rheological factors.
Animals↗
Is there any difference in coronary heart disease risk factors and prevalence of fatty liver in subjects with normal body mass index having different physiques?
Levels of coronary heart disease (CHD) risk factors such as systolic and diastolic blood pressure, fasting blood glucose, hemoglobin A1c, triglyceride, cholesterol, HDL-cholesterol, prevalence of hypertension, abnormal glucose tolerance, hypertriglyceridemia, hypercholesterolemia, low HDL-cholesterol level, and fatty liver in normal body mass index (BMI) subjects with high or low waist/height ratios were investigated in middle aged men (45-54 years, BMI: 22-23.2 kg/m2) undergoing a routine health examination. The subjects were divided into two groups according to whether their waist/height ratios were > or = 0.5 (n = 131) or < 0.5 (n = 121). There was no significant difference in age or BMI between the two groups, however, fasting blood glucose, hemoglobin A1c, triglyceride, cholesterol levels, the prevalence of abnormal glucose tolerance, hypercholesterolemia, fatty liver (30.5% vs. 15.7%, p < 0.01), and morbidity index for CHD risk factors (sum of the five risk factors scored as one point each if present) (1.46 vs. 1.04, p < 0.01) were significantly higher in the high waist/height group. In conclusion, even normal BMI subjects should pay attention to their waist/height ratio because of higher CHD risk factor levels, prevalences, morbidity index for CHD risk factors, and higher prevalence of fatty liver.
Anthropometry↗
Effect of ursodeoxycholic acid on prostaglandin metabolism and microsomal membranes in alcoholic fatty liver.
The aim of the present study was to evaluate the effect of ursodeoxycholic acid (UDCA) on prostaglandin and fatty acid metabolism and the possible relation of these substances to the development of alcoholic fatty liver in rats. The effects of UDCA (40 mg/kg/day, 30 days) were studied in rats pair-fed a high-fat diet (52% of calories as fat) with daily ethanol (4 g/kg/day, 30 days) intragastric intubation. The livers of ethanol-treated animals were characterized by fatty dystrophy. Liver triglyceride and cholesterol ester contents and the activities of serum marker enzymes, alanine aminotransferase and gamma-glutamyltransferase, were significantly increased. Ethanol enhanced phosphoinositol and sphingomyelin content in liver microsomes and lowered prostaglandin E(2) (PGE(2)) concentration in the liver. An increase in the percentage of monoenoic fatty acids and a decrease in the n-6 acid family in liver phospholipids, linoleoyl-CoA desaturase, and PGE(2) synthase activities in liver microsomes were observed in ethanol-treated rats. Treatment with UDCA improved liver morphologic characteristics, decreased triglyceride and cholesterol ester contents, increased the PGE(2) level, and normalized linoleoyl-CoA desaturase and PGE(2) synthase activities, as well as phospholipid and fatty acid patterns in the liver. The activities of the serum marker enzymes were decreased in the ethanol- and UDCA-treated group. Ursodeoxycholic acid lowered the viscosity of the microsomal membrane, as assessed by both fluorescence probe techniques and the saturated/unsaturated fatty acid ratio. We propose that the hepatoprotective effect of UDCA in alcoholic fatty liver is related to the stabilization of microsomal membranes, the prevention of a decrease in essential fatty acids and PGE(2) in the liver, and, probably, an improvement in biochemical processes controlled by PGE(2).
Animals↗
Hepatic origin of triglycerides in fatty livers produced by the continuous intragastric infusion of an ethanol diet.
Male Wistar rats were maintained for 30 days on an independent and continuous intragastric infusion of ethanol and nutritionally defined liquid diet containing only a small amount of corn oil (CO-4.9% calories). Ethanol intake was progressively increased from 32% to 40.4% of the total calories to maintain a high degree of intoxication during this period. Rats in the control group were infused with an isocaloric diet in which alcohol was replaced by dextrose. The liver triglyceride (TG) content of rats given alcohol (61.5 +/- 16.4 mg/g) was ca. 10-fold greater than that of controls (5.9 +/- 2.1 mg/g) and similar to that observed previously in rats fed an ethanol diet containing high levels of fat (35% and 43% calories). In TG of fatty liver, the level of 18:2 was small (3%), even though CO in the diet contained a high level of this acid. Furthermore, 16:1 and 16:0 contents were markedly elevated (16% and 40%, respectively) despite the fact that CO did not contain 16:1 and had only a small amount of 16:0. Liver TG having a fatty acid (FA) composition markedly different from that of CO and the presence of high levels of 16:1 and 16:0 indicate that the TG accumulated in the fatty liver originated from hepatic lipogenesis rather than from dietary fat.
Animals↗
Mitochondrial fatty acid oxidation and acute fatty liver of pregnancy.
Accumulation of micro- and macrovesicular fat in hepatocytes is the hallmark of several liver diseases of pregnancy, including acute fatty liver of pregnancy (AFLP) and severe pre-eclampsia. While the exact origin of AFLP is not known, this pathologic finding and its similarity to the hepatopathology found in infants and children with inborn errors of mitochondrial fatty acid-oxidation suggests a common pathogenesis. Over the last few years, the incidence of AFLP and other severe complications of pregnancy have been found to be increased in women who carry a fetus with a defect in fatty acid oxidation, and who are themselves carriers of a genetic mutation that partially compromises their own intramitochondrial fatty acid oxidation pathway. This article reviews evidence that links AFLP with both genetic and acquired factors that compromise intramitochondrial fatty acid oxidation. Based on this review, recommendations are offered for obstetric, perinatal, and neonatal management of affected mothers and infants.
Acute Disease↗
Calcium and its relationship to excess feed consumption, body weight, egg size, fat deposition, shell quality, and fatty liver hemorrhagic syndrome.
In Experiment 1, Hyline W36 caged hens were fed diets containing 1.7, 2.9, 3.5, and 4.1% calcium for 10 and 16 weeks. In Experiments 2 and 4, Dekalb XL and Hyline W36 pullets were fed diets containing 1.0, 1.7, and 3.75% calcium for 3 weeks (Exp. 2) or until 25 pullets from each group laid 7 eggs (Exp. 4). In Experiment 3 and 5, Dekalb and Hyline hens were fed diets containing 1.5 (Dekalb only), 1.75, 2.25, 2.75, and 3.75% calcium for 8 weeks. Criteria were liver, fat pad, egg and shell weights, egg specific gravity, production, feed consumption, liver fat and fatty acid composition, liver hemorrhage score, and body weight. As percent dietary calcium decreased, Hyline birds (Exp. 1, 4, and 5) had increased liver fat, body weight (except Exp. 4), and feed consumption, but egg specific gravity and shell weight decreased. Reduced dietary calcium levels had no effect on egg production in Experiment 1 but significantly reduced production in Experiment 5. Liver hemorrhage score significantly increased as percent dietary calcium decreased (Exp. 1). As dietary calcium decreased, Dekalb pullets (Exp. 2) had increased feed consumption, fat pad weight, and liver hemorrhage score. There was no increase in liver fat. However, in Dekalb hens (Exp. 3), feed consumption and egg production were significantly decreased as dietary calcium decreased. It is concluded that overconsumption caused by feeding pullets or hens inadequate calcium had no beneficial effect on egg size or egg production and, depending on strain, increased liver fat, liver hemorrhage score, body weight, and fat pad weight.
Adipose Tissue↗
Early perivenular sclerosis in alcoholic fatty liver: an index of progressive liver injury.
Alcoholic steatosis was associated with sclerosis around the terminal hepatic venules in liver biopsies of 40% of chronic alcoholics but not in those of moderate drinkers. To determine whether this sclerosis could be a precursor lesion of cirrhosis, controlled studies were performed in animal models. In the alcohol-fed baboons that developed fibrosis or cirrhosis, progressive perivenular sclerosis invariably started at the fatty liver stage before or even more commonly in the absence of alcoholic hepatitis. No sclerosis occurred in controls or in alcohol-fed baboons and rats that did not progress beyond the fatty liver stage. The clinical and experimental data indicate that sclerosis around the terminal venules, a common but often overlooked complication of alcoholic fatty liver, reflects heavy prolonged drinking, and may identify those patients who are susceptible to develop the more advanced lesions of alcoholic liver injury upon continued drinking.
Adult↗
Fatty liver in H63D homozygotes with hyperferritinemia.
To study the clinical correlates of the H63D mutation we have analysed the phenotype of H63D homo-zygotes identified through mutation analysis in a referral laboratory. A total of 366 blood samples referred for HFE analysis were screened for C282Y and H63D mutations. Four H63D homozygotes were identified. All had raised serum ferritin but normal transferrin saturation. They were negative for hepatitis B and C and only one patient consumed excess alcohol. In all 4 cases ultrasonography revealed fatty liver. In two patients a liver biopsy was done and showed mild siderosis with an unusual distribution and macrovesicular steatosis. These data confirm the association between fatty liver, hyperferritinaemia and increased hepatic iron, but do not clarify whether siderosis was related to steatosis rather than homozygosity for the H63D mutation. Patients with fatty liver may complicate the interpretation of data in population studies of the expression of H63D homozygosity.
Adult↗
Beta-hexosaminidase activity in alcoholic fatty liver and in CCl4-induced liver fibrosis of the rat.
beta-Hexosaminidase (Hex) activity was previously found to be increased in the sera of patients with liver cirrhosis, cholestasis and acute alcohol intoxication, as well as in rats with CCl4-induced liver cirrhosis. We studied this enzymatic activity in the sera and liver tissue of rats with alcoholic fatty liver due to prolonged alcohol intake and CCl4-induced liver fibrosis in association with moderate alterations in liver function tests. Serum and liver Hex activity did not show any significant change in both experimental models. These data suggest that Hex is not an alcohol-induced enzyme, and that severe, but not moderate, liver damage can determine the increase in this lysosomal enzymatic activity.
Alanine Transaminase↗
Isolation and characterization of two distinct forms of liver fatty acid binding protein from the rat.
Liver fatty acid binding protein (L-FABP) appears to contain several different forms that may result from post-translational modification or bound ligand. To further assess this possibility, L-FABP was purified from rat liver homogenate and two putative isoforms separated using a sulfonyl column, a strong cation exchange resin. Fraction I eluted at 0.2 M NaCl, had a pI of 7.59, and following a final size exclusion step contained > 98% L-FABP. Fraction II eluted at 1.0 M NaCl, had a pI of 7.59, and following a final size exclusion step contained > 99% L-FABP. Both fractions contained approx. 0.15 moles of endogenous bound fatty acid per mole of protein, while L-FABP not subjected to the cation exchange step contained 0.75 moles of fatty acid per mole of protein. Fractions I and II had a greater proportion of saturated and monounsaturated fatty acids with a large reduction in polyunsaturated fatty acids compared to L-FABP not fractionated by cation exchange. Mass spectral analysis indicated the molecular mass of Fraction I was 14,315.02 +/- 0.35 Da and Fraction II was 14,315.86 +/- 0.34 Da. The peptide map for each fraction was determined by limited digestion of each fraction with either trypsin, Asp-N, or chymotrypsin to yield overlapping peptide fragments. Mass spectral analysis of these digests indicated the two proteins had identical amino acid fragments and that Cys69 was reduced and there were no Asn to Asp exchanges. Hence, these two forms of L-FABP were not isoforms and were not the result of differences in bound fatty acid. It is proposed that these two distinct forms of rat L-FABP were structural conformers based on two alternative folding pathways.
Amino Acid Sequence↗
The effect of methionine, thiouracil, dienestrol diacetate and thyroprotein on the development and prevention of fatty liver in pullets.
The effect of two levels each of methionine (0.0 and 0.07 percent), thiouracil (0.0 and 0.05 percent), dienestrol diacetate (0.0 and 0.007 percent), and thyroactive casein (0.0 and 0.0125 percent) on the performancy, organ changes, and liver composition in 640 pullets of two strains was studied in a 24 factorial arrangement of treatments. Egg production, egg characteristics, feed conversion, organ weights, and liver composition were parameters measured. Supplemental methionine increased the phosphorus content of liver fat in strain A, but other parameters in the two strains were mot affected by the increase in dietary methionine. The thiouracil increased weight grains, gram of fat per total liver, percent of liver fat, thyroid weight, and heart weight but decreased the phosphorus content of liver fat. Nine typical cases of fatty liver syndrome with large liver hematomas occurred in the thiouracil treated birds and one case occurred in an untreated pullet. Dienestrol diacetate did not affect egg production, egg characteristics, organ weights, and liver composition in the two strains. Thyroprotein decreased weight gain, abdominal fat, liver weight. liver fat, thyroid weight, and percent red cells, but decreased percent blood sports in eggs and adjusted weights of the kidney and heart in both strains.
Adipose Tissue↗