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At least 883 records · Page 49Linked to original sources
PubMed2005

Conjugated linoleic acid-induced fatty liver can be attenuated by combination with docosahexaenoic acid in C57BL/6N mice.

We investigated the effect of dietary combination of conjugated linoleic acid (CLA) and docosahexaenoic acid (DHA) to attenuate CLA-induced fatty liver in C57BL/6N mice. Mice were fed semisynthetic diets that contained either 6% high linoleic safflower oil (HL-SAF), 4% HL-SAF + 2% CLA, or 3.5% HL-SAF + 2% CLA + 0.5% DHA for 4 weeks. This 4 week feeding of CLA showed hepatic lipid accumulation concomitant with the decrease in adipose tissue weight in mice. However, 0.5% supplementation of DHA to the CLA diet could alleviate fatty liver without decreasing the antiobesity effect of CLA. The CLA diet promoted fatty acid synthesis in the liver, but DHA supplementation significantly attenuated the increase in enzyme activity induced by CLA. On the other hand, serum adipocytokines, leptin and adiponectin, were drastically decreased by CLA feeding, and DHA supplementation did not affect those levels. These results show that DHA supplementation to the CLA diet can attenuate CLA-induced fatty liver through the reduction of hepatic fatty acid synthesis without affecting adipocytokine production in C57BL/6N mice.

Animals↗
PubMed1997

Effect of high-fat cholesterol enriched diets on hypolipemic action of Oenothera paradoxa oil in rats. Part 2. Blood serum and liver fatty acids.

The effect of Oenothera paradoxa oil on blood serum and liver fatty acids composition in rats was studied. Rats were fed high-fat diets containing 15% of lard or sunflower oil with or without 0.5% of cholesterol. Soybean protein isolate (27%) was the source of proteins. Intake of Oe. paradoxa oil resulted in increase of levels of gamma-linolenic acid (GLA) and linoleic acid (LA) in blood serum and liver of experimental animals. The effect of Oe. paradoxa oil on blood serum and liver fatty acids composition depended mainly on the type and to the lower degree on the amount of fat in a diet. The addition of cholesterol did not change the influence of examined oil on the composition of fatty acids.

Animals↗
PubMed2005

Dietary conjugated linoleic acid alleviates nonalcoholic fatty liver disease in Zucker (fa/fa) rats.

Nonalcoholic fatty liver disease (NAFLD) is the preferred term to describe the spectrum of liver damage ranging from hepatic steatosis to steatohepatitis, liver fibrosis, and cirrhosis, and it is emerging as the most common liver disease in industrialized countries. Thus, the discovery of food components that would ameliorate NAFLD is of interest. Conjugated linoleic acid (CLA), a mixture of positional and geometric isomers of linoleic acid, has attracted considerable attention because of its potentially beneficial biological effects both in vitro and in vivo. We tested whether dietary CLA protects Zucker (fa/fa) rats from hepatic injury. After 8 wk of feeding, hepatomegaly, hepatic triglyceride (TG) accumulation, and elevated hepatic injury markers in plasma were markedly alleviated in CLA-fed Zucker rats compared with linoleic acid-fed (control) rats. These effects were attributed in part to the enhanced hepatic activities of carnitine palmitoyltransferase, a key enzyme of fatty acid beta-oxidation, and microsomal TG transfer protein, an important factor for lipoprotein secretion due to the CLA diet. We previously reported that the severe hyperinsulinemia in control Zucker rats was attenuated in CLA-fed rats due to an enhanced level of plasma adiponectin, which improves insulin sensitivity. In the present study, the adiponectin concentration was increased and the mRNA expression of tumor necrosis factor-alpha, an inflammatory cytokine, was markedly suppressed in the liver of CLA-fed Zucker rats. We speculate that the enhanced level of liver adiponectin may prevent the development and progression of NAFLD in CLA-fed Zucker rats.

Adiponectin↗
PubMed1984

Stereochemistry of the reactions catalyzed by chicken liver fatty acid synthase.

The stereochemistry of the four partial reactions catalyzed by chicken liver fatty acid synthase that lead to the synthesis of palmitic acid has been determined. The reduction of acetoacetyl-CoA to 3-hydroxybutyryl-CoA by NADPH proceeds with the transfer of the pro-4S hydrogen of NADPH to form D-3-hydroxybutyryl-CoA. During the subsequent dehydration of D-3-hydroxybutyryl-CoA the pro-2S hydrogen and the 3-hydroxyl group are removed in a syn elimination to form crotonyl-CoA. Crotonyl-CoA is reduced to butyryl-CoA by NADPH, with the transfer of the pro-4R hydrogen of NADPH to the pro-3R position in butyryl-CoA and the transfer of a solvent hydrogen to the pro-2S position. The occurrence of the syn dehydration, when combined with the results of a previous study [ Sedgwick , B., & Cornforth , J. W. (1977) Eur. J. Biochem. 75, 465-479], implies that the condensation of the enzyme-bound malonyl moiety with the enzyme-bound saturated fatty acid to form a 3-keto intermediate proceeds with inversion at C-2 of the malonyl. The stereochemistry of the hydration was derived from an analysis of the spin-spin coupling constant of 3-hydroxy[2-2H]butyric acid benzylamides obtained from 3-hydroxy[2-2H]butyryl-CoA synthesized by fatty acid synthase. The elucidation of the stereochemistry of the reduction of crotonyl-CoA relied on the previously established stereochemistry of pork liver acyl-CoA dehydrogenase. The source of all 28 prochiral hydrogens of the palmitic acid synthesized by chicken liver fatty acid synthase was inferred from the results of this work.

Acyl Coenzyme A↗
PubMed2005

Increased hepatocellular uptake of long chain fatty acids occurs by different mechanisms in fatty livers due to obesity or excess ethanol use, contributing to development of steatohepatitis in both settings.

Long chain fatty acids (LCFA) enter cells by both facilitated transport and diffusion, the former accounting for > or = 90%. Facilitated LCFA transport is up-regulated in adipocytes from obese rats, mice, and humans. To clarify the role of hepatocellular LCFA uptake in hepatic steatosis (fatty liver), [3H]-oleic acid (OA) uptake was studied in hepatocytes isolated from Zucker fatty(Z) and control(C) and ethanol-fed(E) Wistar rats, and demonstrated both saturable and non-saturable components, each a function of the unbound OA concentration ([OAu]). The uptake Vmax was identical in C and Z animals, but was increased 2.4-fold in E animals (p < 0.01). The non-saturable uptake rate constant did not differ between groups. Plasma LCFAs averaged 600 microM in C and E and 1,200 microM in Z animals. Total LCFA uptake averaged 1.35, 2.78 and 3.54 pmol/sec/50,000 cells in C, Z, and E animals, respectively. A 2-fold uptake increase in Z animals, in which Vmax was unaltered, entirely reflected the increased plasma LCFA concentration, whereas the 2.6-fold increase in E animals, in which plasma LCFA were not increased, resulted from up-regulation of facilitated transport. Thus, while increased hepatic LCFA uptake contributes to pathogenesis of hepatic steatosis in both obesity and excessive ethanol consumption, the mechanisms differ.

Animals↗
PubMed1984

Effect of diisopropyl 1,3-dithiolan-2-ylidenemalonate on experimental fatty livers in chicks.

The effect of diisopropyl 1,3-dithiolan-2-ylidenemalonate (NKK-100) on experimental fatty livers was investigated in chicks administered an antithyroid agent plus synthetic estrogen or in estrogenized, starved-refed chicks. NKK-100 was added at levels of 250, 500, 1000, and 1500 mg/kg diet. Liver weight was significantly decreased by administration of NKK-100 at 1500 mg/kg diet in the estrogen-administered chicks. Liver lipid content and liver lipid deposition were significantly and inversely decreased with increasing NKK-100 concentration in the diet in the estrogen administered chicks. Plasma transaminase activity, which was elevated by the estrogen administration, was reduced by the administration of NKK-100. These results suggest that NKK-100 may be of value in preventing fatty livers in poultry.

Animals↗
PubMed1985

Human liver fatty acid binding protein. Isolation of a full length cDNA and comparative sequence analyses of orthologous and paralogous proteins.

We have determined the primary structure of human liver fatty acid binding protein from an analysis of a full length cDNA. This 127-residue 14,178-Da protein exhibits a high degree of sequence conservation when compared to its orthologous homologue, rat liver fatty acid binding protein. It appears likely that this polypeptide arose from two intragenic duplication events. Using a variety of computational techniques, we were unable to find any evidence of amphipathic alpha helical domains in this protein nor any sequence similarities to apolipoproteins and serum albumins. A family of paralogous proteins was defined, whose members share a remarkable degree of sequence homology with share a remarkable degree of sequence homology with human liver fatty acid binding protein. These include rat intestinal fatty acid binding protein, the cellular the P2 protein of myelin. It appears that the small cytosolic fatty acid binding proteins have evolved structural features necessary for lipid-protein interaction which are different from those present in some familiar and better studied extracellular sequences.

Amino Acid Sequence↗
PubMed1994

Acute fatty liver of pregnancy: a clinical study of 12 episodes in 11 patients.

Twelve episodes of acute fatty liver of pregnancy (AFLP) were diagnosed in 11 patients during the past 18 years in a general hospital in Santiago, Chile, with a prevalence of 1 per 15,900 deliveries. Acute fatty liver of pregnancy started between the 31st and 38th weeks of pregnancy, with malaise, vomiting, jaundice, and lethargy as the main clinical manifestations. Polydipsia (in nine episodes) and skin pruritus (in seven episodes) were unusual clinical findings. In two patients, pruritus started two and four weeks before AFLP, suggesting that an intrahepatic cholestasis of pregnancy preceded AFLP in those patients. Considering the current prevalence of both diseases in Chile, their association should be considered fortuitous. In another patient, two consecutive pregnancies were affected by AFLP, raising to three the number of reported patients with recurrent AFLP. In 11 episodes, liver biopsies supported the diagnosis of AFLP by showing small and midsized vacuolar cytoplasmic transformation as the most prominent histopathological feature. Positive intracellular fat staining was found in the four samples analysed. Studies by electron microscopy showed megamitochondria with paracrystalline inclusions in four samples. All the mothers survived, but fetal mortality was 58.3%. Several extrahepatic complications delayed maternal recovery for up to four weeks after delivery. This study confirms an improvement in maternal prognosis in AFLP, discusses the possibility of an epidemiological association with intrahepatic cholestasis of pregnancy, and increases the number of patients reported with recurrent AFLP.

Acute Disease↗
PubMed2006

Protective effect of Arthrospira maxima on fatty acid composition in fatty liver.

BACKGROUND: Arthrospira maxima has been widely used for nutritional purposes. Additionally, A. maxima has shown immunomodulator, antiviral, antioxidant, vasomotor and hypolipidemic effects in laboratory and animal studies. A. maxima prevents fatty liver induced by either carbon tetrachloride (CCl4) or fructose-rich diet; however, the liver lipid composition in these models is not clearly known yet. The aim of this study was to evaluate the effects of A. maxima on the liver lipid profile in CCl4-induced steatohepatitis. METHODS: A single sublethal, intraperitoneal dose of CCl4 was administered to male Wistar rats fed a diet with or without 5% A. maxima. Liver lipids: total lipids, triacylglycerols, total cholesterol, free fatty acids, and thiobarbituric acid reactive substances were assessed 24 and 48 h after injury with CCl4. Additionally, triacylglycerols, total cholesterol and aspartate aminotransferase were evaluated in blood. RESULTS: Forty eight hours after CCl4 treatment, rats fed a diet without A. maxima had serum aspartate aminotransferase and liver triacylglycerols values that were, respectively, 2.2 and 1.4 times higher than those of animals receiving 5% A. maxima in their diet. The same pattern was observed for liver free fatty acids and thiobarbituric acid reactive substances. The groups fed a diet with A. maxima and treated with CCl4 showed a higher saturated fatty acid liver content than the groups without A. maxima in their diet. The percentage of unsaturated fatty acids increased 48 h after CCl4 treatment, but its value was 0.5 times lower in the group receiving A. maxima than in the group fed without A. maxima. In the liver, all animals receiving A. maxima showed a trend towards a lower percentage of unsaturated fatty acids, despite the mentioned increase 48 h after CCl4 treatment. CONCLUSIONS: The results suggest that, in the fatty liver induced by CCl4, the hepatoprotective effect of A. maxima involves (a) an antioxidant mechanism and (b) a lower unsaturation of the liver fatty acids. The preventive effect of A. maxima on the liver lipid changes induced by CCl4 could be partially explained by its antioxidant action and the ability to increase the synthesis/release of nitric oxide, but not by its soluble dietary fiber.

Animal Feed↗
PubMed1989

Hypertension does not stimulate the development of hypercholesterolemia or fatty liver induced by a high cholesterol/cholate diet in rats.

A high cholesterol/cholate diet induced hypercholesterolemia and fatty liver in both spontaneously hypertensive rats (SHR) and normotensive control rats (WKY). However, in contrast to previous concepts, the levels of cholesterol ester, triacylglycerol and phosphatidylcholine in plasma as well as triacylglycerol in liver were higher in WKY than in SHR fed a normal diet. The high cholesterol/cholate diet elevated the levels of plasma cholesterol, plasma cholesterol ester and hepatic triacylglycerol, and the extent of elevation was significantly higher in WKY than in SHR. Increases both in monoene/saturated ratios, an indication of elevated delta 9-desaturase activity, and in linoleate/arachidonate ratios, a possible indication of impaired desaturation-elongation activity, were observed in hepatic and plasma lipids of both strains fed the high cholesterol/cholate diet. The increases in monoene/saturated ratios were similar in both strains, but the increases in the linoleate/arachidonate ratios were higher for the plasma cholesterol esters of WKY than of SHR. The n-6/n-3 ratios of plasma and hepatic lipids were higher in WKY than in SHR throughout the experiments. These diet-induced changes observed in hepatic and plasma lipids were not reflected in the aortic lipids. Thus, hypertension per se does not promote the development of hyperlipemia and fatty liver induced by a high cholesterol/cholate diet. Our results also suggest that the metabolism of polyenoic fatty acids is different between SHR and WKY.

Animals↗
PubMed1999

Amino acids in rinse effluents as a predictor of graft function after transplantation of fatty livers in rats.

There are too few reliable markers by which one can predict future function of a liver before implantation. Consequently, the purpose of this study was to test the hypothesis that amino acids in rinse-effluents could predict transplant outcome in marginal fatty livers from rats. Amino acids were measured in the rinse effluent from the livers immediately after harvest and graft preparation or cold storage. Amino acids in the effluent were twice as high in ethanol-treated animals compared to those in nonfatty controls. Ethanol-treated fatty livers survived for no longer than 7 days after transplantation while 83% of nonfatty controls survived (P < 0.05). In subsequent studies, the cold-storage time was decreased to 6 h to determine whether failing fatty livers released more amino acid than grafts that would function normally. There was a significant increase in amino acids in the effluent of fatty grafts compared to controls. Moreover, the sum of the four selected amino acids (alanine, valine, histidine, leucine) was lower than 23 nmol/g liver in functional livers, whereas failing grafts had totals significantly higher than 25 nmol/g liver. The sum of the four amino acids correlated well with 24 h post-transplant serum AST levels (r = 0.78, P < 0.0001). So we can conclude that amino acid release can serve as a useful marker of graft viability and reliably predicts survival.

Alanine Transaminase↗
PubMed2006

[Insulin resistance in non-alcoholic fatty liver disease].

Insulin resistance is the pathophysiological hallmark of various kinds of clinical diseases, including non- alcoholic fatty liver disease. Insulin resistance is the common characteristic of metabolic syndrome and its related features. Insulin resistance is a systemic disease that affects the nervous system, muscles, pancreas, kidney, heart and immune system, in addition to the liver. A complex interaction between genes and environment factors enhances insulin resistance and the phenotypic expression of NAFLD (non- alcoholic fatty liver disease) in individual patients. Advanced fibrotic liver disease is associated with many features of metabolic syndrome, and the risk of progressive liver disease should not be underestimated for the individuals suffering with metabolic disorders. Abnormalities of insulin signaling can cause the state of insulin resistance, but there is no clear cut scientific evidence that distorted insulin signaling is the primary pathophysiological defect. Increased adipose tissue mass can cause peripheral tissue insulin resistance via the changes of the adipocytokine secretory patterns. We discuss in this article the sequences of the insulin signaling cascades and the possible molecular targets of insulin resistance, the humoral "cross talk" between the distorted secretory patterns of the adipocytokines, and the peripheral tissue insulin resistance along with the pathophysiology of NAFLD.

Adipose Tissue↗
PubMed1995

Time trends of plasma lipids and enzymes synthesizing hepatic triacylglycerol during postpartum development of fatty liver in dairy cows.

We studied development of fatty liver in high producing dairy cows with free access to feed during the dry period and thus showed the combined effects of parturition and prepartum overfeeding. Postpartum liver triacylglycerol concentrations at 1 wk postpartum, as measured in liver biopsies, had increased more than 6-fold, which was preceded or accompanied by an increase in plasma NEFA concentrations. Concentrations of hepatic phospholipid changed only slightly. The amounts of total lipids in serum, very low density lipoproteins, and high density lipoproteins significantly decreased by .5 wk after parturition, and concentrations of high density lipoproteins rose steadily. The pattern was similar for concentrations of total cholesterol and phospholipid in serum. Total lipid concentrations in low density lipoproteins were not altered after parturition. The activity of microsomal phosphatidate phosphohydrolase in the liver showed a transient increase at .5 wk after calving, but activity of microsomal glycerolphosphate acyltransferase remained relatively constant. The activities of diacylglycerol acyltransferase had increased about twice at 1 wk after calving and remained at this high level until at least 4 wk after parturition. The rise in activity of diacyglycerol acyltransferase was probably a response to the extra influx of fatty acids to channel them into triacylglycerol. Activities of microsomal cholinephosphate cytidylyltransferase initially increased after calving and then decreased slightly. Activities of hepatic choline kinase had increased after calving. This study indicates that hepatic triacylglycerol accumulates because of the increased hepatic uptake of NEFA and the simultaneous increase in activity of diacylglycerol acyltransferase.

Acyltransferases↗
PubMed2004

Lack of common mutation in the alfa-subunit of the mitochondrial trifunctional protein and the polymorphism of CYP2E1 in three Japanese women with acute fatty liver of pregnancy/HELLP syndrome.

BACKGROUND:: Acute fatty liver of pregnancy (AFLP) and the HELLP syndrome are the serious disorders during pregnancy. The aim of this study is to clarify the prevalence of common mutation in the alpha-subunit of the mitochondrial tri-functional protein: hydroxyacyl-CoA dehydrogenase (LCHAD)/3-ketoacyl-CoA thiolase/enoyl-CoA hydratase as well as to determine the correlation with the polymorphism of microsomal cytochrome P4502E1 (CYP2E1) in these conditions. METHODS:: Genomic DNA was extracted from three patients with AFLP/the HELLP syndrome. Exon 15 of LCHAD and 5'-flanking lesion of CYP2E1 was amplified by PCR and analyzed by RFLP with either of Pst I or the combination of Pst I and Rsa I, respectively. RESULTS:: None of the patients demonstrated the 1528G-C mutation in LCHAD gene. All the patients had homozygous wild-type genotype (c1/c1) in the 5'-flanking lesion of CYP2E1. CONCLUSIONS:: Although limited size of study, our observations suggest the low incidence rate of LCHAD common mutation among Japanese patients with AFLP/HELLP syndrome. Moreover, all of the patients had wild-type genotype of CYP2E1 in this study. Considering with the fact that the neonates from these patients has been in good health for at least 6 years from birth, there might be diverse etiologic factors of Japanese patients with AFLP/HELLP syndrome other than reported genetic mutations.

Journal Article↗