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PubMed1979

Mechanism for fatty liver induction in rats fed arginine deficient diets.

Arginine deficiency is known to lead to marked alterations in pyrimidine biosynthesis and the excessive loss of urinary orotic acid. Orotic acid feeding is known to lead to hepatic steatosis. These studies show that arginine deficiency also results in a marked increase in liver lipids in the rat. The majority of the increased liver lipid can be accounted for by triglyceride accumulation. Increased liver lipid infiltration was found to be independent of the sex of the rat. Accompanying this increase was a decrease in serum triglycerides and cholesterol concentrations. Fatty infiltrations induced by arginine deficiency could be reversed by refeeding an arginine enriched diet. Adenine supplementation (0.30%) to the arginine deficient diet also completely prevented the induction of fatty livers. Adenine supplementation resulted in a dramatic increase in urinary orotic acid excretion in the arginine deficient rat. Guanine supplementation (0.5%) to an arginine deficient diet reduced but did not prevent the induction of fatty livers. The similarities of fatty livers induced by arginine deficiency and orotic acid feeding are discussed.

Adenine↗
PubMed2006

Non-alcoholic fatty liver disease may not be a severe disease at presentation among Asian Indians.

AIM: To evaluate the clinical and biochemical profile of patients with non alcoholic fatty liver disease (NAFLD) and to assess their histological severity at presentation. METHODS: Consecutive patients presenting to the liver clinic of All India Institute of Medical Sciences (AIIMS) with raised transaminases to at least 1.5 times upper limit of normal, and histologically confirmed non-alcoholic fatty liver disease were included. Patients who had significant alcohol intake or positive markers of other liver diseases or who were taking drugs known to produce fatty liver were excluded. The clinical, biochemical and histological profile of this group was studied. RESULTS: Fifty-one patients with NAFLD formed the study population. Their median age and BMI were 34(17-58) years and 26.7(21.3-32.5) kg/m(2) respectively and 46 (90.1%) were males. The majority of the patients had mild inflammation, either grade 1 [32 (63%)] or grade 2 [16 (31%)] and only 3 (6%) patients had severe (grade 3) inflammation. Twenty-three (45%), 19 (37%), 8(16%) and 1(2%) patient had stage 0, 1, 2 and 3 fibrosis respectively on index biopsy and none had cirrhosis. On univariate analysis, triglyceride levels more than 150 mg % (OR = 7.1; 95% CI: 1.6-31.5, P = 0.002) and AST/ALT ratio>1 (OR = 14.3; 95% CI: 1.4-678.5, P = 0.008) were associated with high grades of inflammation and none was associated with advanced fibrosis. On multivariate logistic regression analysis, hypertriglyceridemia >150 mg% was the only factor independently associated with presence of high grade of inflammation (OR = 1.6; 95% CI: 1.3-22.7, P = 0.02), while none was associated with advanced fibrosis. Triglyceride levels correlated positively with inflammatory grade (r = 0.412; P = 0.003). CONCLUSION: NAFLD in North Indian patients is a disease of young over-weight males, most of whom are insulin resistant and they tend to have a mild histological disease at presentation.

Adolescent↗
PubMed1987

Hypocalcemic crisis in alcoholic fatty liver: transient hypoparathyroidism due to magnesium deficiency.

Hypocalcemic crisis developed in a patient with acute alcoholic fatty liver. In addition to jaundice and marked hepatomegaly, the patient presented with hypocalcemic crisis associated with hypomagnesemia, low plasma 1,25(OH)2-vitamin D and undetectable plasma parathyroid hormone (PTH) concentration. Subsequent computerized tomographic scan and liver biopsy showed the presence of severe fatty liver. With the improvement of liver function, the serum calcium level increased, and was accompanied by normalization of plasma PTH, serum magnesium, and plasma 1,25(OH)2-vitamin D levels. Serial ethylenediaminetetraacetic acid infusion tests demonstrated the reversal of the impaired PTH secretion. Thus, hypocalcemic crisis in this patient appeared to result from transient hypoparathyroidism induced by magnesium deficiency.

Acute Disease↗
PubMed1979

[Treatment of alcoholic toxic fatty liver. A placebo-controlled trial with hepavis (author's transl)].

A placebo-controlled double-blind study of 30 patients with advanced chronic fatty liver was intended to show how far treatment with a liver preparation, in this case Hepavis, is superior to alcohol abstinence alone. Examination of the laboratory parameters, especially of gamma GT shows that treatment with Hepavis with simultaneous withdrawal of alcohol produces a rapid normalization or improvement of the laboratory findings and consequently an accelerated improvement in the course of the disease. This leads to the conclusion that the pathological activity of the liver cell is reduced more quickly by the constituents of Hepavis than without suitable therapy, and that a more favorable prognosis for the fatty liver as a potential precurser of cirrhosis is to be attained. Not only is elimination of the lipogenic factor, alcohol, essential in the treatment of fatty liver, but also treatment with hepatotropic substances.

Adult↗
PubMed1984

Cloning of DNA complementary to rat liver fatty acid synthetase mRNA.

Clones, containing DNA complementary (cDNA) to rat liver fatty acid synthetase mRNA, were constructed and identified. cDNA of these clones was then used as a probe to quantify mRNA. The cDNA was synthesized to partially purified rat liver fatty acid synthetase mRNA. Double-stranded cDNA was then prepared and inserted into the PstI site of pBR322 using oligo(dG) X oligo(dC) tailing. Initial selection of the clones was by differential colony hybridization employing [32P]cDNA synthesized from poly(A)-rich mRNA, enriched and non-enriched in fatty acid synthetase mRNA, as probes. Plasmids, containing specific sequences complementary to the fatty acid synthetase mRNA, were identified by hybrid-arrest translation. Cloned cDNA inserts ranged from 300 to 1400 base pairs. Cloned cDNA was employed to probe for mRNA in hybridizations via the dot-blot method. These studies demonstrated an increase in fatty acid synthetase mRNA during dietary induction, which suggests that regulation may involve changes in transcription or changes in post-transcriptional processing of the mRNA.

Animals↗
PubMed2004

Mechanism of hepatic insulin resistance in non-alcoholic fatty liver disease.

Short term high fat feeding in rats results specifically in hepatic fat accumulation and provides a model of non-alcoholic fatty liver disease in which to study the mechanism of hepatic insulin resistance. Short term fat feeding (FF) caused a approximately 3-fold increase in liver triglyceride and total fatty acyl-CoA content without any significant increase in visceral or skeletal muscle fat content. Suppression of endogenous glucose production (EGP) by insulin was diminished in the FF group, despite normal basal EGP and insulin-stimulated peripheral glucose disposal. Hepatic insulin resistance could be attributed to impaired insulin-stimulated IRS-1 and IRS-2 tyrosine phosphorylation. These changes were associated with activation of PKC-epsilon and JNK1. Ultimately, hepatic fat accumulation decreased insulin activation of glycogen synthase and increased gluconeogenesis. Treatment of the FF group with low dose 2,4-dinitrophenol to increase energy expenditure abrogated the development of fatty liver, hepatic insulin resistance, activation of PKC-epsilon and JNK1, and defects in insulin signaling. In conclusion, these data support the hypothesis hepatic steatosis leads to hepatic insulin resistance by stimulating gluconeogenesis and activating PKC-epsilon and JNK1, which may interfere with tyrosine phosphorylation of IRS-1 and IRS-2 and impair the ability of insulin to activate glycogen synthase.

Animals↗
PubMedDate not supplied

Treatment of nonalcoholic fatty liver disease.

Treatment of patients with nonalcoholic fatty liver disease (NAFLD) has typically been focused on the management of associated conditions such as obesity, diabetes mellitus and hyperlipidemia. NAFLD associated with obesity may resolve with weight reduction, although the benefits of weight loss have been inconsistent. Appropriate control of glucose and lipid levels is always recommended, but not always effective in reversing the liver condition. Results of pilot studies evaluating ursodeoxycholic acid, gemfibrozil, betaine, N-acetylcysteine, vitamin E (alpha-tocopherol), metformin and thiazolidinedione derivatives suggest that these medications may be of potential benefit for patients with NAFLD. These medications, however, need first to be tested in well-controlled trials with clinically relevant end-points and extended follow up. A better understanding of the pathogenesis and natural history of NAFLD will help to identify the subset of patients at risk of progressing to advanced liver disease, and hence, those patients who should derive the most benefit from medical therapy.

Diabetes Complications↗
PubMedDate not supplied

Metastatic tumors in irregular fatty liver mimicking focal sparing.

Two cases of hepatic metastatic tumor occurring in irregular fatty liver are reported. These metastatic tumors appeared as irregularly shaped hyperdense areas and were difficult to distinguish from focally spared areas of irregular fatty liver. Even if areas of focal sparing are irregular in shape, hepatic tumors should be carefully ruled out in patients at high risk for liver tumors.

Adult↗
PubMed1987

The role of microtubules in chlorinated alkane-induced fatty liver.

The effect of carbon tetrachloride (CCl4) and methylene chloride (MC) on the hepatic microtubular system and its relationship to the development of fatty liver were examined. Hepatic microtubule content was assessed using a specific colchicine-binding assay. These studies demonstrated that these 2 chlorinated methanes had no early effect on hepatic microtubule content. A significant decrease in microtubules was not observed until after the development of the fatty liver. In vitro tubulin polymerization studies demonstrated that neither CCl4 nor MC had a significant effect on lag-time before tubulin assembly, rate of assembly or the maximum amount of polymerization achieved. It is concluded that an impairment in hepatic microtubule assembly is not responsible for the development of the chlorinated alkane-induced fatty liver.

Animals↗
PubMed1995

Primary nonfunction of fatty livers produced by alcohol is associated with a new, antioxidant-insensitive free radical species.

The formation of free radicals after orthotopic liver transplantation in the rat correlates with graft failure. Fatty livers from alcoholics transplant poorly, so these studies were designed to examine the effect of alcohol on free radical formation in a rearterialized rat liver transplantation model. Treatment of rats for 3-5 weeks with either a high-fat or an ethanol-containing liquid diet caused characteristic pericentral lipid accumulation. After storage in University of Wisconsin cold storage solution (UW) and transplantation, a reperfusion injury characterized by increased postoperative AST levels (greater than 1500 U/l in about 3 hours) was observed in rats fed high-fat or alcohol-containing diets, whereas parenchymal cell injury was seen much less in low-fat controls. Survival was around 63% in the low-fat group but decreased to 12 and 18% in the high-fat and alcohol groups, respectively. Furthermore, intracellular lipid content correlated inversely with survival. In untransplanted livers, the spin trap alpha-phenyl N-tert-butylnitrone (PBN) was infused, and blood samples were collected and extracted with chloroform:methanol. Signals indicative of carbon-centered PBN radical adducts were barely detectable in all untransplanted groups studied by electron paramagnetic resonance. In contrast, a robust 6-line complex spectrum was obtained from all groups studied immediately after 48 hours of cold storage in UW solution and transplantation. A mixture of 3 radical species was identified. Two had coupling constants similar to lipid-derived free radicals, whereas the third is a new species with unique coupling constants and is most likely oxygen derived. In low-fat controls, the signal was reduced significantly by superoxide dismutase (SOD)/catalase; however, SOD/catalase had no effect on free radicals in lipid-loaded livers. Thus, both dietary high fat and alcohol exposure produce a unique SOD/catalase-insensitive free radical species that may be involved in the mechanism of failure of fatty livers after orthotopic liver transplantation.

Alcoholism↗
PubMed2004

Acute fatty liver of pregnancy associated with pancreatitis: a life-threatening complication.

OBJECTIVE: Inadequate data describe pancreatitis as a complication in women with acute fatty liver of pregnancy. Our purpose was to report our experience with this complication, which included maternal and perinatal outcomes. STUDY DESIGN: Medical records of patients with acute fatty liver of pregnancy and/or pancreatitis were reviewed over a 15-year period. Records were reviewed for symptoms, laboratory findings, clinical course, and maternal and perinatal outcomes. RESULTS: Persistent nausea and vomiting were the symptoms in 10 of 12 patients (83%). The average maternal age was 26.3 years (range, 21-37 years). There were two maternal deaths (17%); one death occurred despite liver transplantation. Maternal morbidity included encephalopathy (50%), acute respiratory distress syndrome (17%), and renal failure (33%) that resulted from acute tubular necrosis (3 cases) and acute cortical necrosis (1 case) that required renal transplantation. Of the 12 patients, 11 patients (91%) had an elevated serum lipase level, and another patient had an elevated serum amylase level (9%). Eight of 12 patients (67%) underwent radiologic studies, of which 7 patients (88%) were diagnostic for pancreatitis. Radiographic and autopsy findings noted pancreatic inflammation (3 cases), pseudocyst formation (3 cases), and hemorrhagic pancreatitis (1 case). The radiographic and serum laboratory abnormalities occurred after the onset of hepatic and renal abnormalities in all cases. CONCLUSION: Pancreatitis is a potentially lethal complication of acute fatty liver of pregnancy, and all patients with this diagnosis should undergo screening for the abnormality. Pancreatic abnormalities typically appear after hepatic and renal dysfunction.

Acute Disease↗
PubMed1977

Changes in plasma lipid and glucose levels during the onset of fatty liver and kidney syndrome in chics.

Plasma glucose, free fatty acid and triglyceride levels were measured during the onset of fatty liver and kidney syndrome in chicks. Intial studies indicated that behavioural and clinical changes characteristically associated with the syndrome were observed only during the 24 h preceding death. A more detailed examination of the blood changes was made on fasted birds. Typically, affected birds could be distinguished from healthy fasted birds by a hypoglycaemia which developed within 2.5 h of the removal of food, and a slightly higher and more sustained elevation of free fatty acid levels. Triglyceride values were not generally different from those found in normal birds. Although moderate to large amounts of lipid were occasionally observed in the kidneys of healthy fasted birds, only in affected birds was significant lipid infiltration of the kidneys associated with a similar level of lipid infiltration of the liver. In extreme cases death from fatty liver and kidney syndrome could occur within 4 h of the removal of food.

Animals↗
PubMed1988

The diagnosis of acute fatty liver of pregnancy by computed tomography.

We describe 2 patients with biopsy-proven acute fatty liver of pregnancy in whom the diagnosis was suggested by the finding of uniform reduced attenuation values on computed tomography (CT) of the liver. The attenuation values returned to normal with resolution of signs and symptoms following delivery. CT of the liver provides a useful method for the diagnosis of acute fatty liver of pregnancy.

Acute Disease↗
PubMed1990

Laparoscopic findings of fatty liver using multiple regression analysis. "Spotty" and "diffuse" yellow color.

Laparoscopic features of fatty liver including the cases with fibrotic change were studied by multiple regression analysis. The coloration of the liver surface under laparoscopy was classified into three types: "spotty" yellow color (YC) type, "diffuse" YC type, and without YC type. The presence of YC on the liver surface depended on the amount of deposited lipid (standardized estimate = 0.606, p = 0.0001). However, the presence of YC and whether it appeared "spotty" or "diffuse" was independent of the intralobular distribution and size of the deposited lipid droplets. When YC was observed in cases without fibrotic change, 19 of the 23 with more than 30% lipid droplets in the biopsy specimens had "spotty" YC. When YC was found in cases with fibrotic change, all of the 14 cases with more than 30% lipid droplets were "diffuse" YC. A linear regression model showed that the yellow colored liver with fibrotic change had a "diffuse" appearance (yes = 1, no = 0) standardized estimate = 0.569, p = 0.0009). These data suggested that the amount of lipid deposited was responsible for the presence of YC on the liver surface both with and without fibrotic change, and that the co-existence of fibrotic change was a major factor for giving the yellow colored liver a "diffuse" appearance.

Biopsy↗
PubMed1991

Interpretation of patho-physiology by laboratory data (4). Cases of hypernutritional fatty liver.

Using blood chemistry data from 77 cases of hypernutritional fatty liver diagnosed in our gastroenterological clinic, an automated quantitative interpretation was formulated. The reliability of this interpretation was confirmed in view of the following points: 1) Comparison with the degree of fatty infiltration of the liver seen in biopsy specimens or ultrasonographic findings. 2) The high rate of coincidence, sensitivity and specificity among the results. 3) Localization of almost all the cases of fatty or non-fatty liver into circumscribed areas by the value of standard deviation index (SDI) of glutamic oxaloacetic transaminase (GOT) i.e. aspartate aminotransferase (AST) and cholinesterase (CHE), respectively. 4) Graphic display of data and interpretation of a representative case of acute hepatitis at specified stages, and the comparison of this interpretation with clinical diagnoses and course of the disease. Moreover, two possible mechanisms for the elevation of the CHE level were discussed.

Adult↗
PubMed2006

High sensitivity of fatty liver Shionogi (FLS) mice to diethylnitrosamine hepatocarcinogenesis: comparison to C3H and C57 mice.

The fatty liver Shionogi (FLS) mouse is a new inbred strain that spontaneously develops fatty liver with infiltration of mononuclear cells. Moreover, this mouse is known to frequently develop spontaneous hepatic cancers. Recently, human non-alcholic steatohepatitis (NASH) has been focused of attention regarding hepatocellular carcinoma. Therefore, this mouse has potential as a model for human hepatic cancer due to steatosis. It is of interest therefore, whether it exhibits elevated susceptibility not only regarding spontaneous tumor development but also to chemical hepatocarcinogens. To examine this concern, we examined diethylnitrosamine (DEN) hepatocarcinogenesis in FLS mice with 30ppm in drinking water for 26 weeks in comparison to two other strains of mice, C3H and C57. The induction of spontaneous and DEN-induced hepatic tumors was clearly increased in the FLS case, along with levels of 8-hydroxy-2'-deoxyguanosine (8-OHdG), a marker of oxidative DNA damage, as compared to the other strains, with or without DEN treatment. These results indicate that the oxidative DNA stress is intimately involved in hepatocarcinogenesis in FLS mice and provide further support for use of this mouse as a useful model for investigating hepatocarcinogenesis due to human hepatic steatosis.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2004

Metabolic significance of nonalcoholic fatty liver disease in nonobese, nondiabetic adults.

BACKGROUND: Obesity and type 2 diabetes are well-known risk factors for the development of nonalcoholic fatty liver disease (NAFLD). However, NAFLD is not rare in nonobese, nondiabetic adults. The aim of this study was to evaluate the metabolic significance of NAFLD in nonobese, nondiabetic adults. METHODS: This study examined 768 nonobese (body mass index [BMI] [calculated as weight in kilograms divided by the square of height in meters], > or =18.5 and <30) (460 normal-weight and 308 overweight subjects), nondiabetic individuals older than 30 years who participated in a medical checkup. All the subjects had negative serologic findings for hepatitis B and C viruses and had an alcohol intake less than 140 g/wk. A standard interview, anthropometrics, a biochemical study, and abdominal ultrasonography were conducted. RESULTS: The prevalence of NAFLD in the enrolled subjects was 23.4%. In the normal-weight (BMI, > or =18.5 and <25) and overweight (BMI, > or =25 and <30) groups, NAFLD was a significant predictor of insulin resistance and other metabolic disorders, including hypertriglyceridemia and hyperuricemia. The odds ratio of the metabolic disorders in subjects with NAFLD compared with those without NAFLD in the normal-weight group was higher than that in the overweight group. Multiple logistic regression analysis showed that sex, waist circumference, triglyceride level, and insulin resistance were independently associated with NAFLD in the normal-weight group. CONCLUSIONS: Nonalcoholic fatty liver disease is closely associated with metabolic disorders, even in nonobese, nondiabetic subjects. Nonalcoholic fatty liver disease can be considered an early predictor of metabolic disorders, particularly in the normal-weight population.

Adult↗
PubMed1992

Free fatty acid transfer from rat liver fatty acid-binding protein to phospholipid vesicles. Effect of ligand and solution properties.

Fatty acid binding proteins (FABP) are a family of 14-15-kDa proteins found in many mammalian cell types in high abundance. Although their precise physiological role remains hypothetical, the transfer of free fatty acids (ffa) to intracellular membrane sites is believed to be an important function of FABP. To better understand the role of FABP in this process, we have examined how the rate of ffa transfer from liver FABP (L-FABP) to model membranes is influenced by variations in ffa structure and properties of the aqueous phase. The rate of transfer of fluorescent anthroyloxy ffa to model acceptor membranes was monitored using a resonance energy transfer assay. The results show that a monounsaturated ffa transfers 2-fold more rapidly than a saturated ffa of equivalent chain length, and a two-carbon increase in acyl chain length results in a 3-fold decrease in transfer rate. The transfer rate decreases logarithmically with increasing ionic strength, suggesting that the aqueous solubility of the ffa is an important determinant of its dissociation rate from L-FABP. Fatty acid binding and the relative partition of n-(9-anthroloxy) ffa to L-FABP as compared with phospholipid membranes both decrease as pH decreases, indicating that ionized but not protonated ffa bind to L-FABP. The rate of ffa transfer from L-FABP to membranes increases approximately 4-fold with increasing pH, suggesting that ionization of the ffa carboxyl group is also an important determinant of the transfer process. Analysis of the dependence of the transfer rate on temperature demonstrates that the delta G++ of the activated state for ffa transfer arises from both enthalpic and entropic processes. These studies demonstrate that the rate of transfer of long chain ffa from L-FABP to membranes is substantially affected by aqueous phase variables as well as properties of the ffa ligand itself.

Animals↗