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PubMed1978

Lipid metabolism in laying hens. The relationship of plasma lipids and liver fatty acid synthetase activity to changes in liver composition.

Plasma and liver samples were taken from a random sample of caged commercial hybrid layer hens which had been in egg production for fifteen months. The concentration of plasma and liver lipids and the activity of liver fatty acid synthetase (FAS) were measured in laying hens with liver weight of 20 to 53 g. Liver total lipid, water, non-lipid, and cytosolic fractions, which are the four major liver components, increased linearly with respect to wet liver weight. FAS activity increased with all liver components. Accumulation of lipid in the liver did not inhibit FAS activity. Total cholesterol, free cholesterol, esterified cholesterol, triglycerides, and phosphorous were measured on each plasma sample. Multiple regression analysis showed that all plasma lipids, except cholesterol esters, were related cubically with increasing wet liver weight and cytosolic protein.

Animals↗
PubMed1989

[Study of microcirculatory changes in experimental dietary fatty liver].

UNLABELLED: Regional hepatic blood flow in SD rats with fatty liver was measured by electrolytic regional blood flow meter (Biomedical Sci. Co. Ltd. model RBF-2) and compared with areas of sinusoids histologically calculated by CONTRON MOP-AM 03. METHODS: SD male rats, weighing around 240 g, fed on the choline deficient diet, were anaesthetized with ethyl ether and rough regional hepatic blood flow were measured after 3, 5 and 7 weeks. Furthermore, after 15 min. from death, they were measured (death regional flow) in order to determine the simple diffusion of hydrogen gas in liver tissue. Real regional blood flow was got by subtraction of death regional flow from rough regional blood flow. The degree of fatty liver was histologically divided into 3 groups, as it were, slight, moderate and severe. The lipid was extracted from fatty liver in 3 groups using the combined liquids of methanol and chloroform, and the weight of the lipid was measured to compare with fatty changes. The area of sinusoids in fatty liver was analyzed from microscopic pictures using CONTRON MOP-AM 03. RESULTS: There was no difference of rough regional hepatic blood flow among 3 groups as shown Figure.: (table; see text) But the real regional blood flow was decreased in the moderate or severe groups. And the lipid weights of the liver tissues were increased according to severe fatty changes. The values of real regional blood flow were well-correlated with decrease of the areas of sinusoids histologically analyzed. These facts suggested that fat vacuoles narrowed the lumen of sinusoid and decreased the hepatic blood flow.

Animals↗
PubMed1997

9-cis-retinoic acid enhances fatty acid-induced expression of the liver fatty acid-binding protein gene.

The role of retinoic acids (RA) on liver fatty acid-binding protein (L-FABP) expression was investigated in the well differentiated FAO rat hepatoma cell line. 9-cis-Retinoic acid (9-cis-RA) specifically enhanced L-FABP mRNA levels in a time- and dose-dependent manner. The higher induction was found 6 h after addition of 10(-6) M 9-cis-RA in the medium. RA also enhanced further both L-FABP mRNA levels and cytosolic L-FABP protein content induced by oleic acid. The retinoid X receptor (RXR) and the peroxisome proliferator-activated receptor (PPAR), which are known to be activated, respectively, by 9-cis-RA and long chain fatty acid (LCFA), co-operated to bind specifically the peroxisome proliferator-responsive element (PPRE) found upstream of the L-FABP gene. Our result suggest that the PPAR-RXR complex is the molecular target by which 9-cis-RA and LCFA regulate the L-FABP gene.

Alitretinoin↗
PubMed2003

Ablation of the liver fatty acid binding protein gene decreases fatty acyl CoA binding capacity and alters fatty acyl CoA pool distribution in mouse liver.

Although liver fatty acid binding protein (L-FABP) is known to bind not only long chain fatty acid (LCFA) but also long chain fatty acyl CoA (LCFA-CoA), the physiological significance of LCFA-CoA binding has been questioned and remains to be resolved. To address this issue, the effect of L-FABP gene ablation on liver cytosolic LCFA-CoA binding, LCFA-CoA pool size, LCFA-CoA esterification, and potential compensation by other intracellular LCFA-CoA binding proteins was examined. L-FABP gene ablation resulted not only in loss of L-FABP but also in concomitant upregulation of two other intracellular LCFA-CoA binding proteins, acyl CoA binding protein (ACBP) and sterol carrier protein-2 (SCP-2), by 45 and 80%, respectively. Nevertheless, the soluble fraction from livers of L-FABP (-/-) mice bound 95% less radioactive oleoyl-CoA than wild-type L-FABP (+/+) mice. The intracellular LCFA-CoA binding protein fraction (Fraction III) from wild-type L-FABP (+/+) mice, isolated by gel permeation chromatography of liver soluble proteins, exhibited one high-affinity binding and several low-affinity binding sites for cis-parinaroyl-CoA, a naturally occurring fluorescent LCFA-CoA. In contrast, high-affinity LCFA-CoA binding was absent from Fraction III of L-FABP (-/-) mice. While L-FABP gene ablation did not alter liver LCFA-CoA pool size, LCFA-CoA acyl chains of L-FABP (-/-) mouse livers were enriched 2.1-fold in C16:1 and decreased 1.9-fold in C20:0 fatty acids. Finally, L-FABP gene ablation selectively increased the amount of LCFAs esterified into liver phospholipid > cholesteryl ester, while concomitantly decreasing the amount of fatty acids esterified into triglycerides by 40%. In summary, these data with L-FABP (-/-) mice demonstrated for the first time that L-FABP is a physiologically significant contributor to determining liver cytosolic LCFA-CoA binding capacity, LCFA-CoA acyl chain distribution, and esterified fatty acid distribution.

Acyl Coenzyme A↗
PubMed1997

Effect of growth hormone on fatty liver in panhypopituitarism.

A 17 year old boy was admitted because of short stature and hepatomegaly. He was diagnosed with panhypopituitarism and fatty liver. The fatty liver improved, not with hydrocortisone or levothyroxine treatment, but with growth hormone administration. The fatty liver in this patient was attributable to a growth hormone deficient state.

Adolescent↗
PubMed2006

Relationship between in vivo chlorzoxazone hydroxylation, hepatic cytochrome P450 2E1 content and liver injury in obese non-alcoholic fatty liver disease patients.

The aim of the present study was to test the hypothesis that induction of cytochrome P450 2E1 (CYP2E1) in the liver of patients with non-alcoholic fatty liver disease (NAFLD) is correlated both with the in vivo activity of the cytochrome and with the development of liver injury. For this purpose, the liver content of CYP2E1 was determined by Western blot and the CYP2E1 activity by the in vivo hydroxylation of chlorzoxazone (CLZ). The study groups were obese women with an average body mass index (BMI) of 40.3kg/m(2), who underwent therapeutic gastroplasty or gastrectomy with a gastro-jejunal anastomosis. Further, the hepatic histology was determined to establish the pathological score grouping the subjects into three categories: control, steatosis and steatohepatitis. The liver CYP2E1 content and the CLZ hydroxylation of obese patients with steatosis and, particularly, with steatohepatitis were significantly higher than controls and correlated positively with both the severity of the liver damage. These data provide evidence that CYP2E1 would be involved in the mechanism of liver injury found in obese NAFLD patients. Also, the correlation between liver CYP2E1 content and in vivo CLZ hydroxylation would validate the latter as a reliable indicator of liver injury in NAFLD, thus providing a simple and not invasive method to study these patients.

Journal Article↗
PubMed1997

Diffuse fatty liver in familial heterozygous hypobetalipoproteinemia.

A 34-year-old man had asymptomatic hepatomegaly, slightly increased serum alanine aminotransferase and gamma-glutamyl transpeptidase levels, and a sonographic pattern suggesting diffuse hepatic steatosis. Liver biopsy revealed fatty change in 25% to 50% of hepatocytes. The patient also had low serum levels of cholesterol and triglycerides and met clinical, biochemical, and familial diagnostic criteria of heterozygous hypobetalipoproteinemia. We could not relate his hepatic steatosis to any already known cause of fatty liver and could only attribute it to heterozygous hypobetalipoproteinemia. Familial heterozygous hypobetalipoproteinemia should be ruled out in patients with unexplained hepatic steatosis.

Adult↗
PubMed2001

Effects of fatty acids and growth hormone on liver fatty acid binding protein and PPARalpha in rat liver.

The aim of this study was to investigate the interaction between long-chain fatty acids (LCFA) and growth hormone (GH) in the regulation of liver fatty acid binding protein (LFABP) and peroxisome proliferator-activated receptor-alpha (PPARalpha). Cultured rat hepatocytes were given oleic acid (OA; 500 microM) and GH (100 ng/ml) for 3 days. LFABP mRNA increased 3.6-fold by GH and 5.7-fold by OA, and combined incubation with GH and OA increased LFABP mRNA 17.6-fold. PPARalpha mRNA was decreased 50% by GH, but OA had no effect. Hypophysectomized (Hx) female rats were treated with L-thyroxine, cortisol, GH, and dietary fat for 7 days. PPARalpha mRNA levels were three- to fourfold higher in Hx than in normal female rats. GH decreased PPARalpha mRNA 50% in Hx rats. Dietary triglycerides (10% corn oil) increased LFABP mRNA and cytosolic LFABP about twofold but had no effect on PPARalpha mRNA in Hx rats. GH and dietary triglycerides had an additive effect on LFABP expression. Dietary triglycerides increased mitochondrial hydroxymethylglutaryl-CoA synthase mRNA only in the presence of GH. The diet increased serum triglycerides in Hx rats, and GH treatment prevented this increase. Addition of cholesterol to the diet did not influence LFABP levels but mitigated increased hepatic triglyceride content. In summary, these studies show that GH regulates LFABP expression independently of PPARalpha. Moreover, GH has different effects on PPARalpha-responsive genes and does not counteract the effect of LCFA on the expression of these gene products.

Animals↗
PubMed1998

Role of hyperinsulinemia and glucose intolerance in the pathogenesis of nonalcoholic fatty liver in patients with normal body weight.

OBJECTIVES: The pathogenesis of nonalcoholic fatty liver in non-obese persons is poorly understood. We aimed to elucidate whether hyperinsulinemia and glucose intolerance are associated with development of fatty liver in patients with normal body weight. METHODS: Forty-seven patients with fatty liver were divided into non-obese (n = 25) and obese groups (n = 22) according to age adjusted body mass index. Inclusion criteria were as follows: (1) elevated transaminase levels during more than 3 months of follow up period, (2) no detectable HBsAg or anti-HCV in the serum, (3) alcohol consumption less than 40 gm/week, (4) no use of potential hepatotoxic drugs within 3 months and (4) sonographic evidence of fatty liver(moderate to severe degree). Baseline insulin levels and oral glucose tolerance test using 75gm of glucose were performed and the results were compared in each group of patients. RESULTS: Mean baseline insulin levels were elevated in both groups above the reference value, 9.3 +/- 3.5 microU/L in non-obese group and 9.9 +/- 3.5 microU/L in obese group (p = 0.26). Seventeen of non-obese patients (68%) had elevated basal insulin level and 16 of obese patients (73%) had elevated basal insulin level (p = 0.39). In oral glucose tolerance test, there was no difference in glucose level between non-obese and obese groups from O minute to 180 minutes (p > 0.05). Eleven patients from the non-obese group (44%) and 8 patients from the obese group (36%) had either impaired glucose tolerance or diabetes (p = 0.29). CONCLUSION: Our data suggest that hyperinsulinemia and glucose intolerance may play a role in the pathogenesis of fatty liver in patients with normal body weight as well as in patients with obesity.

Adult↗
PubMed2006

[Fatty liver disease and statins--which discipline the problem belongs to?].

While fatty liver disease is a well-characterized entity, it is currently getting a completely new image. Its treatment is clearly an interdisciplinary challenge. The number of patients with fatty liver disease will be by no means negligible. The issue of fatty liver disease is not infrequently referred to in association with statin therapy instituted in an effort to treat metabolic syndrome and to reduce cardiovascular risks as part of preventive therapy. The attention focused on the increase in alanin aminotransferase levels during statin therapy is absolutely inadequate. The study includes an overview of the topic showing the induced rise in alanin aminotransferase is merely an accompanying phenomenon, mostly of no clinical relevance. An acceptable increase in alanin aminotransferase should not provide a reason for statin withdrawal in the usual spectrum of patients with metabolic syndrome and fatty liver disease. A distinct advantage is cooperation among a hepatologist, a cardiologist, and a diabetes expert.

Alanine Transaminase↗
PubMed2003

Oxidative stress and oval cell accumulation in mice and humans with alcoholic and nonalcoholic fatty liver disease.

In animals, the combination of oxidative liver damage and inhibited hepatocyte proliferation increases the numbers of hepatic progenitors (oval cells). We studied different murine models of fatty liver disease and patients with nonalcoholic fatty liver disease or alcoholic liver disease to determine whether oval cells increase in fatty livers and to clarify the mechanisms for this response. To varying degrees, all mouse models exhibit excessive hepatic mitochondrial production of H(2)O(2), a known inducer of cell-cycle inhibitors. In mice with the greatest H(2)O(2) production, mature hepatocyte proliferation is inhibited most, and the greatest number of oval cells accumulates. These cells differentiate into intermediate hepatocyte-like cells after a regenerative challenge. Hepatic oval cells are also increased significantly in patients with nonalcoholic fatty liver disease and alcoholic liver disease. In humans, fibrosis stage and oval cell numbers, as well as the number of intermediate hepatocyte-like cells, are strongly correlated. However, cirrhosis is not required for oval cell accumulation in either species. Rather, as in mice, progenitor cell activation in human fatty liver diseases is associated with inhibited replication of mature hepatocytes. The activation of progenitor cells during fatty liver disease may increase the risk for hepatocellular cancer, similar to that observed in the Solt-Farber model of hepatocarcinogenesis in rats.

Animals↗
PubMed2003

Prostaglandin E1 improved the function of transplanted fatty liver in a rat reduced-size-liver transplantation model under conditions of permissible cold preservation.

The aim of this study was to determine whether the minimum necessary volume of a moderate fatty liver graft was similar to the normal liver volume and to elucidate means for improving the function of the transplanted fatty liver if it were inferior in volume to a normal liver under conditions of permissible cold preservation. Nine-week-old male Wistar rats were used. Normal rat chow was fed to the normal liver group, and fat-enriched rat chow was fed to the fatty liver group for 4 weeks to induce a moderately fatty liver. Liver transplantation with various volumes of reduced-size grafts, including whole liver graft (100%LT), 70% volume graft (70%LT), and 30% volume graft (30%LT), was performed with both groups of rats as donors. All procedures were performed under the conditions of 2-hour cold preservation. All rats with an implanted normal liver were surviving at 7 days after the operation regardless of the graft volume (100%LT, 5 of 5; 70%LT, 5 of 5; 30%LT, 5/5). In contrast, the survival rates decreased according to the graft volume in rats implanted with fatty livers (100%LT, 8 of 8; 70%LT, 5 of 8; 30%LT, 2/8). To improve the survival of 30%LT with fatty liver, we employed two potent inhibitors of ischemia-reperfusion injury: FK506 and prostaglandin E1. Though FK506 had no advantageous effect, prostaglandin E1 significantly improved the survival rate and diminished serum levels of alanine aminotransferase and hyaluronic acid. In conclusion, the volume of graft necessary for successful transplantation is larger in fatty livers than in normal livers in permissible cold preservation. Also, prostaglandin E1 protects grafts against ischemia-reperfusion injury and improves the functioning of a transplanted fatty liver.

Alanine Transaminase↗
PubMed1987

The initial presentation of fatty liver of pregnancy mimicking acute viral hepatitis.

Acute fatty liver of pregnancy, a disease of the 3rd trimester of pregnancy, may have varied presentations. An unusual initial presentation of acute fatty liver of pregnancy mimicking an acute viral hepatitis is reported herein. Osmium tetroxide preparation of pathological specimen for the diagnosis of acute fatty liver of pregnancy is also discussed.

Adult↗
PubMed1996

Fatal fat embolism in acute hepatic necrosis with associated fatty liver.

We report two cases of generalized nonviolent hepatogenic fat embolism. A 63-year-old woman was sent to the hospital with suspected mushroom poisoning. Shock symptoms occurred quickly and could not be treated effectively; the patient died 24 h after admission. Postmortem examination showed acute yellow dystrophy of the liver with a severe preexisting fatty liver. Any intoxication including Amanita phalloides could be excluded. In all probability, a fulminant viral hepatitis caused liver dystrophy, and the decay of the fatty liver cells led to generalized fat embolism as the cause of death. The second patient, a 46-year-old man, was reported to have suffered from an acute illness while in prison and died after having been transferred to the local hospital. Histological examinations showed an acute liver dystrophy probably caused by fulminant viral hepatitis with fatty degeneration. In this case, the cause of death was also found to be generalized fat embolism.

Acute Disease↗
PubMed2001

Oxidative stress in fatty livers of obese Zucker rats: rapid amelioration and improved tolerance to warm ischemia with tocopherol.

Fatty livers in humans and rats are less tolerant of ischemia, endotoxin, and alcohol. We hypothesized that fatty livers of obese (Ob) Zucker rats are oxidatively stressed and oxidative stress could be relieved by antioxidant treatment, leading to improved tolerance to ischemia. Total glutathione (GSH), tocopherol (TOC), ascorbic acid (AA), catalase (CAT), superoxide dismutase (SOD), and selenium-glutathione peroxidase (Se-GPx) were measured in the livers of Ob and lean (Ln) Zucker rats before and after treatment with high-dose TOC and ascorbate. Also, survival in treated Ob rats following a lethal 90 minutes of partial in vivo warm ischemia was examined. Fatty livers of Ob rats contained significantly less GSH, TOC, and CAT, in comparison with livers of Ln rats. Immunoblotting showed significantly decreased CAT protein without changes in mRNA in fatty livers. There were no significant differences in AA, SOD, and Se-GPx between the 2 groups. Pretreatment with TOC and ascorbate over 48 hours completely corrected the decreases in GSH, TOC, and CAT. Most importantly, TOC with or without ascorbate pretreatment significantly improved survival in Ob rats following ischemia in a dose-dependent manner. In conclusion, TOC administration corrected the oxidative stress in fatty livers of Ob Zucker rats and improved survival following lethal ischemia. Additional studies are needed to determine the efficacy of TOC-a relatively inexpensive agent-in treating patients with fatty livers in a variety of clinical conditions, possibly including liver transplantation.

Animals↗
PubMed1975

Induction of fatty liver by ethanol drinking in KK and KK-Ay mice.

Marked fatty liver was found to develop in both KK and KK-Ay (yellow KK) mice when they were allowed free access to a 15% ethanol solution as drinking fluid. The present studies were undertaken to elucidate the characterization of the fatty liver and associated changes. Chemical analysis showed that accumulated lipids were mainly triglycerides, whose fatty acid composition was changed with increases in palmitoleic and oleic acids, indicating augmentation in endogenous lipogenesis. An accumulation of small fat droplets was histologically observed in centrolobular hepatocytes extending to perilobular zones. Among the tested mice of seven strains, only KK and KK-Ay mice developed the ethanol-induced fatty liver, and the latter mice were more susceptible. Growth, food and alcohol intakes, plasma levels of glucose, triglycerides, and immunoreactive insulin were also surveyed during the development of the alcoholic fatty liver. In contrast to high energy diet, ethanol induced neither development of obesity nor exaggeration of diabetic states. A possible correlation between the pathogenesis of the fatty liver and the genetic factor inherited in KK mice is discussed.

Age Factors↗
PubMed2006

Diagnostic value of biochemical markers (FibroTest-FibroSURE) for the prediction of liver fibrosis in patients with non-alcoholic fatty liver disease.

BACKGROUND: Liver biopsy is considered as the gold standard for assessing non-alcoholic fatty liver disease (NAFLD) histologic lesions. The aim of this study was to determine the diagnostic utility of non-invasive markers of fibrosis, validated in chronic viral hepatitis and alcoholic liver disease (FibroTest, FT), in patients with NAFLD. METHODS: 170 patients with suspected NAFLD were prospectively included in a reference center (Group 1), 97 in a multicenter study (Group 2) and 954 blood donors as controls. Fibrosis was assessed on a 5 stage histological scale validated by Kleiner et al from F0 = none, F1 = perisinusoidal or periportal, F2 = perisinusoidal and portal/periportal, F3 = bridging and F4 = cirrhosis. Histology and the biochemical measurements were blinded to any other characteristics. The area under the ROC curves (AUROC), sensitivity (Se), specificity (Sp), positive and negative predictive values (PPV, NPV) were assessed. RESULTS: In both groups FT has elevated and not different AUROCs for the diagnosis of advanced fibrosis (F2F3F4): 0.86 (95%CI 0.77-0.91) versus 0.75 (95%CI 0.61-0.83; P = 0.10), and for F3F4: 0.92 (95%CI 0.83-0.96) versus 0.81 (95%CI 0.64-0.91; P = 0.12) in Group 1 and Group 2 respectively. When the 2 groups were pooled together a FT cutoff of 0.30 had a 90% NPV for advanced fibrosis (Se 77%); a FT cutoff of 0.70 had a 73% PPV for advanced fibrosis (Sp 98%). CONCLUSION: In patients with NAFLD, FibroTest, a simple and non-invasive quantitative estimate of liver fibrosis reliably predicts advanced fibrosis.

Age Factors↗