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Results for “FATTY LIVER”

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PubMed1993

[Evaluation of fatty liver changes and fatty degeneration in liver tumors by 1H-MRS].

This study assesses the ability of 1H-MR spectroscopy (MRS) to evaluate fatty liver changes and fatty degeneration in liver tumors using the STEAM sequence, 1 cm3 VOI, TR/TE/excitations = 600/34/32, during breath-holding. To determine the correlation between lipid group signal ratio (fat fraction (FF)) obtained from in vivo 1H-MRS studies and liver lipid obtained from in vitro measurements (Folch method), an experimental fatty liver model in rabbits was used. Excellent correlation between them (R = 0.94) was noted. The result suggest that fatty liver (over 5% lipid accumulation by weight) is present when the FF by MRS is greater than 3.6%. Thirty-seven liver parenchymal and 18 hepatic tumors (17 hepatocellular carcinomas and 1 cholangiocellular carcinoma) with histological confirmation of the lipid content in 39 patients were examined to assess the clinical utility. Histological fat content was classified into grades 0-4 according to Levinson et al. There was a high correlation between MRS and histology in groups 0 to 2. MRS had a sensitivity of 100%, a specificity of 83% and an accuracy of 86% for diagnosis of "fatty liver" compared to histologic data, whereas CT had a sensitivity of 43%, a specificity of 90%, and an accuracy of 81%. MRS with STEAM sequence appears to be useful method in diagnosis of fatty liver with high sensitivity and accuracy, which is obtained in short time (approximately 7 minutes) and without ionizing radiation exposure.

Animals↗
PubMed1987

Pertussis toxin induces fatty liver, hyperlipemia and ketosis in hamsters.

Pertussis toxin markedly affects lipid metabolism in hamsters. The toxin induces a time-dependent and dose-dependent accumulation of triacylglycerols in the liver (fatty liver) and moderate increases in cholesterol and phospholipids. These toxin produced dramatic increases in the amounts of triacylglycerols, free fatty acids and ketone bodies in the serum and small increases in cholesterol and phospholipids. It is suggested that an enhanced and unregulated lipolysis may play a key role in the induction of these alterations by the toxin.

Acidosis↗
PubMed1983

The influence of environmental temperature, thyroid status and a synthetic oestrogen on the induction of fatty livers in chicks.

1. Hepatic lipid content, lipogenic enzyme activity and plasma lipid concentration were measured in chicks reared at 21 degrees or 34 degrees C and after thyroxine (T4), thiouracil (TU), propylthiouracil (PTU), dienestrol diacetate (DD) or PTU with DD had been given for 14 d. 2. At 34 degrees C there was a significant increase in the total liver lipid and triglyceride content. 3. Injections of T4 decreased liver lipid content whereas it was increased by feeding PTU or DD. The effects of PTU were more pronounced at 21 degrees C while those of DD were more pronounced at 34 degrees C. 4. There were significant interactions between temperature, thyroid status and synthetic oestrogen treatments on total lipid and triglyceride content of the liver. Fatty liver with marked steatosis could be produced through synergic actions of PTU and DD in chicks maintained at 21 degrees C.

Animals↗
PubMed2004

Interleukin 6 alleviates hepatic steatosis and ischemia/reperfusion injury in mice with fatty liver disease.

Fatty liver, formerly associated predominantly with excessive alcohol intake, is now also recognized as a complication of obesity and an important precursor state to more severe forms of liver pathology including ischemia/reperfusion injury. No standard protocol for treating fatty liver exists at this time. We therefore examined the effects of 10 days of interleukin 6 (IL-6) injection in 3 murine models of fatty liver: leptin deficient ob/ob mice, ethanol-fed mice, and mice fed a high-fat diet. In all 3 models, IL-6 injection decreased steatosis and normalized serum aminotransferase. The beneficial effects of IL-6 treatment in vivo resulted in part from an increase in mitochondrial beta oxidation of fatty acid and an increase in hepatic export of triglyceride and cholesterol. However, administration of IL-6 to isolated cultured steatotic hepatocytes failed to decrease lipid contents, suggesting that the beneficial effects of IL-6 in vivo do not result from its effects on hepatocytes alone. IL-6 treatment increased hepatic peroxisome proliferator-activated receptor (PPAR) alpha and decreased liver and serum tumor necrosis factor (TNF) alpha. Finally, 10 days of treatment with IL-6 prevented the susceptibility of fatty livers to warm ischemia/reperfusion injury. In conclusion, long-term IL-6 administration ameliorates fatty livers and protects against warm ischemia/reperfusion fatty liver injury, suggesting the therapeutic potential of IL-6 in treating human fatty liver disease.

Animals↗
PubMed2006

Dietary soya protein concentrate enriched with isoflavones reduced fatty liver, increased hepatic fatty acid oxidation and decreased the hepatic mRNA level of VLDL receptor in obese Zucker rats.

Casein-based diets containing a low (LDI) or high (HDI) dose of soya protein concentrate enriched with isoflavones were fed to obese Zucker rats for 6 weeks. HDI feeding, but not LDI feeding, reduced the fatty liver and decreased the plasma levels of alanine transaminase and aspartate transaminase. This was accompanied by increased activities of mitochondrial and peroxisomal beta-oxidation, acetyl-CoA carboxylase, fatty acid synthase and glycerol-3-phosphate acyltransferase in liver and increased triacylglycerol level in plasma. The decreased fatty liver and the increased plasma triacylglycerol level appeared not to be caused by an increased secretion of VLDL, as HDI decreased the hepatic mRNA levels of apo B and arylacetamide deacetylase. However, the gene expression of VLDL receptor was markedly decreased in liver, but unchanged in epididymal white adipose tissue and skeletal muscle of rats fed HDI, indicating that the liver may be the key organ for the reduced clearance of triacylglycerol-rich lipoproteins from plasma after HDI feeding. The n-3/n-6, 20:4n-6/18:2n-6 and (20:5n-3+22:6n-3)/18:3n-3 ratios were increased in liver triacylglycerol by HDI. The phospholipids in liver of rats fed HDI contained a low level of 20:4n-6 and a high level of 20:5n-3, favouring the production of anti-inflammatory eicosanoids. When obese Zucker rats were fed soya protein, this also resulted in reduced fatty liver, possibly through reduced clearance of VLDL by the liver. We conclude that the isoflavone-enriched soya concentrate as well as soya protein may be promising dietary supplements for treatment of non-alcoholic fatty liver.

Animals↗
PubMed2003

Decreased liver fatty acid binding capacity and altered liver lipid distribution in mice lacking the liver fatty acid-binding protein gene.

Although liver fatty acid-binding protein (L-FABP) is an important binding site for various hydrophobic ligands in hepatocytes, its in vivo significance is not understood. We have therefore created L-FABP null mice and report here their initial analysis, focusing on the impact of this mutation on hepatic fatty acid binding capacity, lipid composition, and expression of other lipid-binding proteins. Gel-filtered cytosol from L-FABP null liver lacked the main fatty acid binding peak in the fraction that normally comprises both L-FABP and sterol carrier protein-2 (SCP-2). The binding capacity for cis-parinaric acid was decreased >80% in this region. Molar ratios of cholesterol/cholesterol ester, cholesteryl ester/triglyceride, and cholesterol/phospholipid were 2- to 3-fold greater, reflecting up to 3-fold absolute increases in specific lipid classes in the order cholesterol > cholesterol esters > phospholipids. In contrast, the liver pool sizes of nonesterified fatty acids and triglycerides were not altered. However, hepatic deposition of a bolus of intravenously injected [14C]oleate was markedly reduced, showing altered lipid pool turnover. An increase of approximately 75% of soluble SCP-2 but little or no change of other soluble (glutathione S-transferase, albumin) and membrane (fatty acid transport protein, CD36, aspartate aminotransferase, caveolin) fatty acid transporters was measured. These results (i) provide for the first time a quantitative assessment of the contribution of L-FABP to cytosolic fatty acid binding capacity, (ii) establish L-FABP as an important determinant of hepatic lipid composition and turnover, and (iii) suggest that SCP-2 contributes to the accumulation of cholesterol in L-FABP null liver.

Acetyl-CoA C-Acetyltransferase↗
PubMed2005

Comparison of the natural history of alcoholic and nonalcoholic fatty liver disease.

Fatty liver disease represents a common clinical entity. It is classically divided into alcoholic fatty liver disease (AFLD) and nonalcoholic fatty liver disease (NAFLD). Whereas AFLD occurs in as many as 10 million Americans, NAFLD represents the most common chronic liver disease and is the most common cause of liver enzyme abnormalities in the United States. Both diseases encompass the clinical spectrum of steatosis, steatohepatitis, and cirrhosis. Although they are histologically indistinct, AFLD and NAFLD follow different clinical courses. This article compares the natural history of these diseases.

Biopsy, Needle↗
PubMed2006

Exogenous glucagon effects on health and reproductive performance of lactating dairy cows with mild fatty liver.

Severe fatty liver, a metabolic disease of dairy cows in early lactation, results in decreased health and reproductive performance, but can be alleviated by treatment with i.v. injections of glucagon. Mild fatty liver in cows effects on health and reproductive performance were determined by treatment with 14-day s.c. injections of glucagon at 7.5 or 15 mg/day. Multiparous Holstein cows (n=32) were grouped into Normal and Susceptible based on liver triacylglycerol concentrations (>1% liver tissue biopsy wet weight) at day 8 postpartum (day 0=day of parturition). Susceptible cows (n=24) were assigned randomly to three groups and s.c. injected with 0mg glucagon [60 ml 0.15M NaCl] [n=8] (same for Normal cows), 2.5 mg glucagon, or 5 mg glucagon every 8 h for 14 days, beginning day 8 postpartum. Mild fatty liver resulted in an increased number of days with elevated body temperature during the injection period, an increased incidence of mastitis after glucagon treatment, increased days to first estrus and insemination, increased days before conception occurred, and decreased conception rate. In cows with mild fatty liver, glucagon (15 mg/day) decreased the number of days with elevated body temperature and the incidence of mastitis after hormone treatment. From these results, we suggest that mild fatty liver is detrimental to health and reproduction of dairy cows and, furthermore, that exogenous glucagon decreases some of these detrimental effects.

Animals↗