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PubMed1976

Biotin deficiency and fatty liver and kidney syndrome in chicks given purified diets containing different fat and protein levels.

1. The occurence of biotin deficiency and fatty liver and kidney syndrome (FLKS) in chicks was studied using a 2x2x2x2 factorial-design experiment in which the variables were dietary biotin, fat and protein, and starvation. 2. The severity of biotin deficiency, using growth retardation and severity of dermal lesions as criteria, was least when the low-biotin diet also contained low levels of fat and protein. Addition of fat or protein increased the severity of the deficiency. Tissue fatty acid composition was affected by biotin deficiency only in those birds given the low-protein, low-fat diet. The main change was an increase in the ratio, 16:1 fatty acids :18:0 fatty acids. Plasma glucose and free fatty acid levels in non-fasted birds were unaffected by the dietary variables. 3. Mortality from FLKS with the diet containing low biotin, fat and protein levels was 52% at 28d, but was reduced or eliminated when the dietary level of any of these ingredients was increased. 4. Starvation considerably increased the incidnece of FLKS in the period immediately after fasting, and also affected plasma glucose and free fatty acid concentrations. Liver fatty acid composition, indicated an increase in the proportion of 18:0 at the expense of 16:1 and concentrations increased in proportion, at the expense of 18:0. 5. The relationship between biotin deficiency and FLKS, and a possible mechanism for the induction of FLKS by starvation are discussed.

Adipose Tissue↗
PubMed1990

Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation.

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.

Acute Disease↗
PubMed1991

Fatty liver. Chemical shift phase-difference and suppression magnetic resonance imaging techniques in animals, phantoms, and humans.

In vitro animal and human models were used to evaluate the potential of chemical shift magnetic resonance imaging (MRI) for assessing fatty liver. Phantoms of varying fat content were created from mayonnaise-agar preparations. Fatty liver was induced in eight rats by feeding them ethanol for three to six weeks (36% of total calories), whereas eight control rats were fed a normal diet. T1-weighted in-phase and opposed-phase MR images were obtained of the phantoms animals, and 28 human subjects. Additional images obtained in animals included long TR images with in-phase and opposed-phase technique, and hybrid chemical shift water and fat suppression. The rats were killed and histologic status was graded blindly by a hepatopathologist as normal, mild, moderate, or severe fatty change, for correlation with MR grading. Quantitative analysis of MR images included fat signal fraction for animals, and relative signal decrease between in-phase and opposed-phase images for phantom and human data. Phantom in-phase signal increased linearly with respect to fat content, whereas opposed-phase signal decreased linearly. MRI and histologic grading of rat livers were highly correlated, especially when based on water suppression images (r = 0.91, P = .0001). Opposed-phase images were also highly correlated, while fat suppression images were less effective. There was no overlap between MR-derived fat fractions for control (2.6%-5.7%) versus ethanol-fed rats (7.7%-17.9%, P = .0002). Human liver considered to be fatty by visual inspection (n = 8) had higher relative signal decrease than nonfatty liver (n = 22) (P less than .001). Phantom, animal, and human data demonstrate that comparison of T1-weighted in-phase and opposed-phase images is both practical and sensitive in the detection and grading of fatty liver.

Adult↗
PubMed1982

Liberation, purification, and properties of thioesterase component of pigeon liver fatty acid synthetase complex.

Proteolysis of pigeon liver fatty acid synthetase with elastase results in the quantitative cleavage of the thioesterase component from the enzyme complex. This thioesterase component is two or three times more active catalytically in the isolated state than in the native fatty acid synthetase, and its activity is not affected by the presence or absence of reducing thiols. The proteolytically cleaved thioesterase is separated from the core enzyme in one step by size-exclusion chromatography on a Sephadex G-75 column. The peptide obtained by gel permeation is homogeneous with respect to size and charge, as shown by polyacrylamide gel electrophoresis in the presence and absence of SDS. Size-exclusion chromatography on Bio-Gel A 0.5 m and Sephadex G-75 columns, sucrose density gradient ultracentrifugation, and N-terminal amino acid analysis also indicate that the proteolytically cleaved thioesterase is homogeneous. The sedimentation coefficient of the thioesterase is approximately 2.9 S. Proteolytic cleavage with elastase also quantitatively releases the [1,3-14C]- or [1,3-3H]diisopropylphosphofluoridate-labeled thioesterase component from the correspondingly labeled fatty acid synthetase. Binding studies with 14C- or 3H-labelled diisopropylphosphofluoridate and fatty acid synthetase show that 2 mol of the label are bound per mol of the enzyme when complete loss of fatty acid-synthesizing activity occurs. The molecular weight of the thioesterase component is estimated to be 36000 by size-exclusion chromatography, SDS-polyacrylamide gel electrophoresis and amino acid analysis.

Amino Acids↗
PubMed2024

A functional genomic framework to elucidate novel causal metabolic dysfunction-associated fatty liver disease genes.

BACKGROUND AND AIMS: Metabolic dysfunction-associated fatty liver disease (MASLD) is the most prevalent chronic liver pathology in western countries, with serious public health consequences. Efforts to identify causal genes for MASLD have been hampered by the relative paucity of human data from gold standard magnetic resonance quantification of hepatic fat. To overcome insufficient sample size, genome-wide association studies using MASLD surrogate phenotypes have been used, but only a small number of loci have been identified to date. In this study, we combined genome-wide association studies of MASLD composite surrogate phenotypes with genetic colocalization studies followed by functional in vitro screens to identify bona fide causal genes for MASLD. APPROACH AND RESULTS: We used the UK Biobank to explore the associations of our novel MASLD score, and genetic colocalization to prioritize putative causal genes for in vitro validation. We created a functional genomic framework to study MASLD genes in vitro using CRISPRi. Our data identify VKORC1 , TNKS , LYPLAL1 , and GPAM as regulators of lipid accumulation in hepatocytes and suggest the involvement of VKORC1 in the lipid storage related to the development of MASLD. CONCLUSIONS: Complementary genetic and genomic approaches are useful for the identification of MASLD genes. Our data supports VKORC1 as a bona fide MASLD gene. We have established a functional genomic framework to study at scale putative novel MASLD genes from human genetic association studies.

Humans↗
PubMed2004

Hepatitis C and nonalcoholic fatty liver disease.

Hepatitis C virus (HCV) and nonalcoholic fatty liver disease (NAFLD) are the two most common causes of chronic liver disease in North America. NAFLD represents a spectrum of liver lesions that occur in individuals who either do not consume any alcohol or only consume alcohol in quantities generally considered not to be harmful to the liver. This spectrum consists of isolated hepatic macrovesicular steatosis at one end and nonalcoholic steatohepatitis (NASH) at the other. Hepatic steatosis is present in approximately 50% of the subjects with HCV. Genotype 3 is independently associated with hepatic steatosis. In those with genotype 1 infection, steatosis is associated with features of the metabolic syndrome. The presence of hepatic steatosis correlates with the stage of hepatic fibrosis in patients with HCV. This has been related to the presence of insulin resistance. Hepatic steatosis also adversely affects the virologic response rates to anti-HCV therapy. In this article, we will review the epidemiology of HCV and NAFLD, their impact on each other, and the course of the liver disease in individuals afflicted with both conditions.

Adipocytes↗
PubMed2002

Acute fatty liver in pregnancy.

When confronted with liver abnormalities during the third trimester of pregnancy, one should consider acute fatty liver of pregnancy. The differential diagnosis with (pre-)eclampsia and HELLP syndrome is sometimes difficult. In these cases a liver biopsy is helpful though rarely performed during pregnancy. After delivery of the child the liver test abnormalities will ultimately disappear. Recent publications reveal that a dysfunction in the beta-oxidation of mitochondrial fatty acids may contribute to the aetiology of this rare disorder. We describe a case of acute fatty liver in pregnancy, with liver dysfunction (decreased albumin, prolonged prothrombin time) slowly returning to normal after delivery. Testing for disorders in beta-oxidation of mitochondrial fatty acids did not reveal abnormalities in mother or child.

Acute Disease↗
PubMed1978

Fatty liver in hypervitaminosis A: synthesis and release of hepatic triglycerides.

Feeding large doses (30,000 IU/100 g body wt per day) of vitamin A to young rats for 2 days produced fatty liver, caused a stimulation of oxidation and esterification of [1-14C]palmitate by liver slices, and increased the activity of hepatic palmitoyl-CoA synthetase. Under similar conditions, however, release of hepatic triglycerides into the plasma, as judged from the post-Triton triglyceridemia, remained unaffected. It is indicated by the present findings that excessive intake of vitamin A produces fatty liver by stimulating the synthesis of triglycerides in liver without affecting the rate of secretion of hepatic triglycerides. An involvement of altered oxidation of fatty acids in the liver can also be ruled out because in hypervitaminosis A this process is increased rather than decreased as required for fatty liver production.

Acetoacetates↗
PubMed2005

Racial and ethnic distribution of nonalcoholic fatty liver in persons with newly diagnosed chronic liver disease.

We performed a cross-sectional study of newly diagnosed cases of nonalcoholic fatty liver disease (NAFLD) identified between December 1998 and December 2000 in the Chronic Liver Disease Surveillance Study. We compared the demographic and clinical features of NAFLD in a racially diverse representative U.S. population (Alameda County, CA). Diagnostic criteria for probable NAFLD were persistent unexplained elevation of serum aminotransferase levels, radiology (ultrasound or computed tomography scan) consistent with fatty liver, and/or two or more of the following: (i) body mass index of 28 kg/m(2) or more, (ii) type 2 diabetes, or (iii) hyperlipidemia, in the absence of significant alcohol use. Definite NAFLD cases required histological confirmation. Of the 742 persons with newly diagnosed chronic liver disease, 159 (21.4%) had definite or probable NAFLD. The majority were nonwhite: Hispanics (28%), Asians (18%), African Americans (3%), and other race(s) (6%). African Americans with NAFLD were significantly older than other racial or ethnic groups (P < .001), and in Asians, NAFLD was 3.5 times more common in males than in females (P = .016). Clinical correlates of NAFLD (obesity, hyperlipidemia, diabetes) were similar among racial and ethnic groups, except that body mass index was lower in Asians compared with other groups (P < .001). Compared with the base population (Kaiser Permanente members), Hispanics with NAFLD were overrepresented (28% vs. 10%) and whites were underrepresented (45% vs. 59%). In conclusion, these racial and gender variations may reflect differences in genetic susceptibility to visceral adiposity, including hepatic involvement, and may have implications for the evaluation of persons with the metabolic syndrome. Clinicians need to be aware of the variable presentations of NAFLD in different racial and ethnic groups.

Adult↗
PubMed1993

[Focal fatty liver. A dilemma of differential diagnosis in ultrasonography and CT].

Based on four cases and relevant background literature we partly want to draw attention to the occurrence of focal fatty liver (FFL) and its manifold appearances in connection with ultrasonography (US) and computed tomography (CT), and partly to point out possible pitfalls in US-diagnosis of the liver in cases of extensive fatty liver, where the residual foci of normal liver may incorrectly be interpreted as abnormal lesions. US and CT examination of FFL may cause differential diagnostic problems with risk of misinterpretation and erroneous diagnosis, especially if the phenomenon is unknown. In cases of doubt in US examination, where the uncharacteristic findings together with patient information indicate further examinations, additional CT is first of all recommended. If this still brings no clarity to the diagnosis, the clinical condition in every case will prescribe whether to undertake additional CT after a few weeks or immediately carry out US/CT guided liver biopsy. Current as well as formerly presented research shows that FFL is mainly located in the right hepatic lobe, and possible reasons for that are discussed.

Adult↗
PubMed2005

Non-alcoholic fatty liver disease and insulin resistance.

Non-alcoholic fatty liver disease (NAFLD) is an entity now recognized as one of the leading causes of asymptomatic chronic elevation of aminotransferase levels, which can, however, progress to more advanced forms of hepatic lesion and ultimately to liver failure. Insulin resistance is considered as having a central role in NAFLD pathogenesis, which is related with oxidative stress, abnormal production of cytokines and deregulation of fatty acid metabolism. In this article the authors make a brief review of the epidemiological data about NAFLD and insulin resistance, and their aetiological link, and treatment implications.

Fatty Liver↗
PubMed2002

Arthrospira maxima prevents the acute fatty liver induced by the administration of simvastatin, ethanol and a hypercholesterolemic diet to mice.

An evident fatty liver, corroborated morphologically and chemically, was produced in CD-1 mice after five daily doses of simvastatin 75 mg/Kg body weight, a hypercholesterolemic diet and 20 percent ethanol in the drinking water. After treating the animals, they presented serum triacylglycerols levels five times higher than the control mice, total lipids, cholesterol and triacylglycerols in the liver were 2, 2 and 1.5 times higher, respectively, than in control animals. When Arthrospira maxima was given with diet two weeks prior the onset of fatty liver induction, there was a decrement of liver total lipids (40%), liver triacylglycerols (50%) and serum triacylglycerols (50%) compared to the animals with the same treatment but without Arthrospira maxima. In addition to the mentioned protective effect, the administration of this algae, produced a significant increase (45%) in serum high density lipoproteins. The mechanism for this protective effect was not established in these experiments.

Acute Disease↗
PubMed1983

Acute fatty liver of pregnancy.

Six further cases of acute fatty liver of pregnancy are presented and discussed in relation to the world literature on this rare disease of pregnancy, the aetiology of which is still unknown. The importance of vomiting in late pregnancy is emphasized. A common feature seems to be a metabolic stress, possibly related to infection, which tips a susceptible liver into metabolic failure.

Acute Disease↗
PubMed1975

An ultrastructural and biochemical study of hexachlorophane-induced fatty liver in sheep.

The administration of single or multiple oral doses of hexachlorophane to yearling sheep resulted in a periportal fatty liver. The accumulation of fat is accompanied by ultrastructural changes in the hepatocyte organelles, particularly the endoplasmic reticulum and Golgi apparatus, and by decreased serum lipid and triglyceride levels. It is suggested that an impairment in the triglyceride secretory mechanism of the liver cell may be the patho-physiological basis for fatty liver. However, the changes in the liver were not accompanied by an evidence of significant impairment of liver cell function.

Alcohol Oxidoreductases↗