scholarly journals Astaxanthin lowers plasma TAG concentrations and increases hepatic antioxidant gene expression in diet-induced obesity mice

2014 ◽  
Vol 112 (11) ◽  
pp. 1797-1804 ◽  
Author(s):  
Yue Yang ◽  
Tho X. Pham ◽  
Casey J. Wegner ◽  
Bohkyung Kim ◽  
Chai Siah Ku ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
Plasma Concentrations ◽  
Control Group ◽  
Related Factor ◽  
Mrna Levels ◽  
Alcoholic Fatty Liver ◽  
Antioxidant Genes ◽  
Endogenous Antioxidant

Non-alcoholic fatty liver disease (NAFLD) is significantly associated with hyperlipidaemia and oxidative stress. We have previously reported that astaxanthin (ASTX), a xanthophyll carotenoid, lowers plasma total cholesterol and TAG concentrations in apoE knockout mice. To investigate whether ASTX supplementation can prevent the development of NAFLD in obesity, male C57BL/6J mice (n 8 per group) were fed a high-fat diet (35 %, w/w) supplemented with 0, 0·003, 0·01 or 0·03 % of ASTX (w/w) for 12 weeks. The 0·03 % ASTX-supplemented group, but not the other groups, exhibited a significant decrease in plasma TAG concentrations, suggesting that ASTX at a 0·03 % supplementation dosage exerts a hypotriacylglycerolaemic effect. Although there was an increase in the mRNA expression of fatty acid synthase and diglyceride acyltransferase 2, the mRNA levels of acyl-CoA oxidase 1, a critical enzyme in peroxisomal fatty acid β-oxidation, exhibited an increase in the 0·03 % ASTX-supplemented group. There was a decrease in plasma alanine transaminase (ALT) and aspartate transaminase (AST) concentrations in the 0·03 % ASTX-supplemented group. There was a significant increase in the hepatic mRNA expression of nuclear factor erythroid 2-related factor 2 and its downstream genes, which are critical for endogenous antioxidant mechanism, in the 0·03 % ASTX-supplemented group. Furthermore, there was a significant decrease in the mRNA abundance of IL-6 in the primary splenocytes isolated from the 0·03 % ASTX-supplemented group upon lipopolysaccharide (LPS) stimulation when compared with that in the splenocytes isolated from the control group. In conclusion, ASTX supplementation lowered the plasma concentrations of TAG, ALT and AST, increased the hepatic expression of endogenous antioxidant genes, and rendered splenocytes less sensitive to LPS stimulation. Therefore, ASTX may prevent obesity-associated metabolic disturbances and inflammation.

scholarly journals Molecular characteristic of activin receptor IIB and its functions in growth and nutrient regulation in Eriocheir sinensis

PeerJ ◽  
2020 ◽  
Vol 8 ◽  
pp. e9673
Author(s):  
Jingan Wang ◽  
Kaijun Zhang ◽  
Xin Hou ◽  
Wucheng Yue ◽  
He Yang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Lipid Metabolism ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
Eriocheir Sinensis ◽  
Negative Regulator ◽  
Control Group ◽  
Molting Cycle ◽  
Activin Receptor ◽  
Activin Receptor Iib

Activin receptor IIB (ActRIIB) is a serine/threonine-kinase receptor binding with transforming growth factor-β (TGF-β) superfamily ligands to participate in the regulation of muscle mass in vertebrates. However, its structure and function in crustaceans remain unknown. In this study, the ActRIIB gene in Eriocheir sinensis (Es-ActRIIB) was cloned and obtained with a 1,683 bp open reading frame, which contains the characteristic domains of TGF-β type II receptor superfamily, encoding 560 amino acids. The mRNA expression of Es-ActRIIB was the highest in hepatopancreas and the lowest in muscle at each molting stage. After injection of Es-ActRIIB double-stranded RNA during one molting cycle, the RNA interference (RNAi) group showed higher weight gain rate, higher specific growth rate, and lower hepatopancreas index compared with the control group. Meanwhile, the RNAi group displayed a significantly increased content of hydrolytic amino acid in both hepatopancreas and muscle. The RNAi group also displayed slightly higher contents of saturated fatty acid and monounsaturated fatty acid but significantly decreased levels of polyunsaturated fatty acid compared with the control group. After RNAi on Es-ActRIIB, the mRNA expressions of five ActRIIB signaling pathway genes showed that ActRI and forkhead box O (FoxO) were downregulated in hepatopancreas and muscle, but no significant expression differences were found in small mother against decapentaplegic (SMAD) 3, SMAD4 and mammalian target of rapamycin. The mRNA expression s of three lipid metabolism-related genes (carnitine palmitoyltransferase 1β (CPT1β), fatty acid synthase, and fatty acid elongation) were significantly downregulated in both hepatopancreas and muscle with the exception of CPT1β in muscles. These results indicate that ActRIIB is a functionally conservative negative regulator in growth mass, and protein and lipid metabolism could be affected by inhibiting ActRIIB signaling in crustacean.

scholarly journals Supplementing calcium salts of soybean oil to beef steers early in life to enhance carcass development and quality1

2019 ◽  
Vol 97 (10) ◽  
pp. 4182-4192 ◽  
Author(s):  
Kelsey M Schubach ◽  
Reinaldo F Cooke ◽  
Alice P Brandão ◽  
Osvaldo A de Sousa ◽  
Thiago F Schumaher ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Soybean Oil ◽  
Mrna Expression ◽  
Fatty Acid Synthase ◽  
Carcass Traits ◽  
Plasma Concentrations ◽  
Beef Steers ◽  
Creep Feeding ◽  
Fatty Acid Binding ◽  
Ppar Γ

Abstract This study evaluated the effects of supplementing Ca salts of soybean oil (CSSO) to beef steers at 2 mo of age via creep-feeding, and/or during a 40-d preconditioning period on performance and carcass development responses. A total of 64 steers were enrolled in this study over 2 yr (32 steers per year), with 4 periods each year: creep-feeding (CF; day 0 to 60), preweaning (day 61 to weaning on day 124 and 127 of year 1 and 2, respectively), preconditioning (PC; day 132 to 172 in year 1 and day 135 to 175 of year 2), and feedlot (feedlot arrival to slaughter, day 173 to 378 in year 1 and day 176 to 385 in year 2). On day 0 steers were ranked by body weight (BW) and age (114 ± 4 kg of BW; 66.1 ± 0.9 d of age) and allocated to 1 of 16 pens. Pens were randomly assigned to receive CSSO during CF (80 g/d per steer) and/or PC (150 g/d per steer) in a 2 × 2 factorial arrangement of treatments. During CF and PC, nonsupplemented steers (CON) were provided an isolipidic prilled saturated fat supplement. Steer BW was recorded on day 0, 60, at weaning, and prior to feedlot shipping. Carcass traits were recorded upon slaughter. On day 0, 60, at weaning, prior to feedlot shipping, and during the feedlot period, blood samples were collected and longissimus muscle (LM) biopsies were collected. On day 60, steers that received CSSO during CF had greater (P < 0.01) plasma concentrations of linoleic and ω-6 compared with CON (CF treatment × day; P ≤ 0.05). Steers that received CSSO during PC had greater (P < 0.01) plasma concentrations of linoleic, ω-6, and total fatty acids compared with CON at feedlot shipping (PC treatment × day; P ≤ 0.05). A PC treatment × day interaction was also detected (P = 0.04) for mRNA expression of peroxisome proliferator-activated receptor gamma (PPAR-γ), which was greater (P = 0.04) at feedlot shipping for steers receiving CSSO during PC. Interactions between CF treatment × day were detected (P ≤ 0.01) for mRNA expression of adipocyte fatty acid-binding protein, fatty acid synthase, PPAR-γ, and stearoyl-CoA desaturase, which were greater (P ≤ 0.02) in the feedlot in steers receiving CSSO during CF. No treatment differences were detected for (P ≥ 0.18) performance or carcass traits, including marbling and backfat thickness. Results from this study suggest that supplementing CSSO to suckled beef steers via creep-feeding upregulated mRNA expression of the adipogenic genes investigated herein later in life. These outcomes, however, were not translated into improved carcass quality.

scholarly journals Manganese influences the expression of fatty acid synthase and malic enzyme in cultured primary chicken hepatocytes

2017 ◽  
Vol 118 (11) ◽  
pp. 881-888 ◽  
Author(s):  
Lin Lu ◽  
Meiling Wang ◽  
Xiudong Liao ◽  
Liyang Zhang ◽  
Xugang Luo
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Malic Enzyme ◽  
Fatty Acid Synthase ◽  
Cell Damage ◽  
Manganese Chloride ◽  
Transcriptional Level ◽  
Mrna Levels ◽  
Expression Levels ◽  
Mrna Expression Levels

AbstractTwo experiments were designed to investigate the effects of Mn source and concentration on the mRNA expression and enzymatic activities of fatty acid synthase (FAS) and malic enzyme (ME) in cultured primary broiler hepatocytes. In Expt 1, primary broiler hepatocytes were treated with 0 (control), 0·25, 0·50 or 0·75 mmol/l of Mn as inorganic manganese chloride (MnCl2.4H2O) for 24 and 48 h. In Expt 2, primary broiler hepatocytes were incubated with 0 (control), 0·25 or 0·50 mmol/l of Mn as either manganese chloride or Mn–amino acid chelate for 48 h. The mRNA levels and activities of FAS and ME in the hepatocytes were measured in Expts 1 and 2. The results in Expt 1 showed that only at 48 h mRNA expression levels of FAS and ME in the hepatocytes decreased linearly (P<0·001) and quadratically (P<0·02) as supplemental Mn concentrations increased. In Expt 2, compared with the control, Mn supplementation reduced (P<0·01) the activities of FAS, mRNA expression levels of FAS and ME in the hepatocytes, and the efflux of lactic dehydrogenase to the medium. The supplemental Mn at 0·5 mmol/l showed a lower (P<0·03) ME mRNA expression level compared with the Mn group at 0·25 mmol/l. However, Mn source and the interaction between Mn source and concentration had no impacts (P>0·33) on any of the measured cellular parameters. The results suggested that Mn might reduce cell damage and regulate FAS and ME expression at a transcriptional level in primary cultured broiler hepatocytes.

scholarly journals Fatty Acid Synthase Inhibitor Platensimycin Intervenes the Development of Nonalcoholic-Fatty Liver Disease in a Mouse Model

Biomedicines ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 5
Author(s):  
Meng Su ◽  
Danfeng Cao ◽  
Zhe Wang ◽  
Yanwen Duan ◽  
Yong Huang
Keyword(s):  
Fatty Acid ◽  
Liver Disease ◽  
Mouse Model ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Fatty Acid Synthase ◽  
Western Diet ◽  
World Population ◽  
Mrna Levels ◽  
Alcoholic Fatty Liver

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease affecting about 25% of world population, while there are still no approved targeted therapies. Although platensimycin (PTM) was first discovered to be a broad-spectrum antibiotic, it was also effective against type II diabetes in animal models due to its ability to inhibit both bacterial and mammalian fatty acid synthases (FASN). Herein, we report the pharmacological effect and potential mode of action of PTM against NAFLD in a Western diet/CCI4-induced mouse model and a free fatty acids (FFAs)-induced HepG2 cell model. The proper dose of PTM and its liposome-based nano-formulations not only significantly attenuated the Western diet-induced weight gain and the levels of plasma total triglycerides and glucose, but reduced liver steatosis in mice according to histological analyses. Western blotting analysis showed a reduced protein level of FASN in the mouse liver, suggesting that PTM intervened in the development of NAFLD through FASN inhibition. PTM reduced both the protein and mRNA levels of FASN in FFAs-induced HepG2 cells, as well as the expression of several key proteins in lipogenesis, including sterol regulatory element binding protein-1, acetyl-CoA carboxylase, and stearoyl-CoA desaturase. The expression of lipid oxidation-related genes, including peroxisome proliferator activated receptor α and acyl-CoA oxidase 1, was significantly elevated. In conclusion, our study supports the reposition of PTM to intervene in NAFLD progression, since it could effectively inhibit de novo lipogenesis.

scholarly journals Maternal obesity markedly increases placental fatty acid transporter expression and fetal blood triglycerides at midgestation in the ewe

2010 ◽  
Vol 299 (5) ◽  
pp. R1224-R1231 ◽  
Author(s):  
Mei J. Zhu ◽  
Yan Ma ◽  
Nathan M. Long ◽  
Min Du ◽  
Stephen P. Ford
Keyword(s):  
Fatty Acid ◽  
Mrna Expression ◽  
Protein Content ◽  
Maternal Obesity ◽  
National Research Council ◽  
Control Group ◽  
Mrna Levels ◽  
Fetal Blood ◽  
Fatty Acid Transporter ◽  
Acid Transporter

Obesity of women at conception is increasing, a condition associated with offspring obesity. We hypothesized that maternal obesity increases placental fatty acid transporter (FATP) expression, enhancing delivery of fatty acids to their fetuses. Sheep are a commonly utilized biomedical model for pregnancy studies. Nonpregnant ewes were randomly assigned to a control group [100% of National Research Council (NRC) recommendations] or obese group (OB, 150% of NRC) from 60 days before conception to 75 or 135 days of gestation (dG; term = 150 dG), when placental cotyledonary tissue was collected for analysis. Fetuses of OB ewes were markedly heavier ( P < 0.05) on 75 dG than fetuses from control ewes, but this difference disappeared by 135 dG. Maternal obesity markedly increased ( P < 0.05) cholesterol and triglyceride concentrations of both maternal and fetal blood. There is no difference in lipoprotein lipase mRNA expression between control and OB group at either gestational age. On 75 dG, the mRNA expression of FATP1 ( P < 0.05), FATP4 ( P = 0.08), and fatty acid translocase CD (cluster of differentiation) 36 ( P < 0.05) proteins were more enhanced in cotyledonary tissue from OB than control ewes; consistently, protein expression of FATP1 and FATP4 was increased ( P < 0.05). Similarly, on 135 dG, the mRNA levels of FATP1, FATP4, and CD36 were all higher ( P < 0.05), but only FATP4 protein content was enhanced ( P < 0.05) in OB cotyledonary tissue. Peroxisome proliferator-activated receptor (PPAR)-γ regulates the expression of FATPs. Both the mRNA expression and protein content of PPARγ were increased in OB cotyledonary in the midgestation. In conclusion, maternal obesity enhances the mRNA expression and protein content of FATPs in cotyledonary in the midgestation, which is associated with higher PPARγ content in cotyledonary.

Insect Meal as Alternative Protein Source Exerts Pronounced Lipid-Lowering Effects in Hyperlipidemic Obese Zucker Rats

2019 ◽  
Vol 149 (4) ◽  
pp. 566-577 ◽  
Author(s):  
Denise K Gessner ◽  
Anne Schwarz ◽  
Sandra Meyer ◽  
Gaiping Wen ◽  
Erika Most ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Cholesterol Biosynthesis ◽  
Control Diet ◽  
Plasma Concentrations ◽  
Protein Source ◽  
Lipid Lowering ◽  
Zucker Rats ◽  
Control Group ◽  
Obese Zucker Rats

ABSTRACT Background Specific dietary proteins exert strong health-related effects compared with casein. Objective Herein, the hypothesis was tested using screening and conventional biochemical and molecular biological techniques that protein-rich insect meal compared with casein influences metabolic health in hyperlipidemic rats. Methods A 4-wk feeding trial with male, 8-wk-old homozygous obese Zucker rats (n = 36) and male, 8-wk-old heterozygous lean Zucker rats (n = 12) was performed. Obese rats were randomly divided into 3 obese groups (OC, OI50, and OI100) of 12 rats each and lean rats served as a lean control group (LC). LC and OC were fed a control diet with 20% casein as protein source, whereas in OI50 and OI100 50% and 100% of the casein, respectively, was replaced isonitrogenously by insect meal from Tenebrio molitor L. All data were analyzed by 1-factor ANOVA, except transcriptomic data which were analyzed by groupwise comparisons with the OC group. Results Transcript profiling revealed a coordinated inhibition by −17% to −521% and −37% to −859% of genes involved in fatty acid, triacylglycerol (TG), and cholesterol biosynthesis in the livers of OI100 and OI50, respectively, compared with OC (P < 0.05). Enzyme activities of fatty acid synthase, glucose-6 phosphate dehydrogenase, and 3-hydroxy-3-methylglutaryl-coenzyme-A reductase in the liver were 100–150% greater in OC compared with LC, but reduced by 50–60% in OI100 compared with OC (P < 0.05), to the same level as in LC. Liver and plasma concentrations of TG and cholesterol were 250–1000%, 30–800%, and 40–600% higher in OC, OI50, and OI100, respectively, than in LC (P < 0.05), but 40–60% and 20–60% lower in OI100 and OI50, respectively, than in group OC (P < 0.05). Plasma and liver concentrations of homocysteine were 20–30% lower in group OI100 than in group OC (P < 0.05). Conclusion Insect meal exerts pronounced lipid-lowering effects in hyperlipidemic rats and, thus, might be useful for hyperlipidemic individuals.

scholarly journals Catechins and Caffeine Inhibit Fat Accumulation in Mice through the Improvement of Hepatic Lipid Metabolism

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Chikako Sugiura ◽  
Shiho Nishimatsu ◽  
Tatsuya Moriyama ◽  
Sayaka Ozasa ◽  
Teruo Kawada ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
Epigallocatechin Gallate ◽  
Acid Synthesis ◽  
Control Group ◽  
Mrna Levels ◽  
Fat Accumulation ◽  
Treatment Groups ◽  
Fas Mrna ◽  
Carnitine Palmitoyltransferase Ii

To elucidate the inhibiting mechanisms of fat accumulation by catechins, caffeine, and epigallocatechin gallate (EGCG), ICR mice were fed diets containing either 0.3% catechins or 0.1% EGCG and/or 0.05% caffeine for 4 weeks. After the feeding, intraperitoneal adipose tissues weights were significantly lower in the caffeine, catechins + caffeine, and EGCG + caffeine groups compared to controls. Hepatic fatty acid synthase (FAS) activity in the catechins + caffeine group was significantly lower, and the activities of acyl-CoA oxidase (ACO) and carnitine palmitoyltransferase-II (CPT-II) were significantly higher, compared to the control group. However, these activities were not observed in the other groups. FAS mRNA expression levels in the catechins + caffeine group were significantly lower than in the control group. ACO and CPT-II mRNA levels were not different among all of the treatment groups. These findings indicate that the inhibitory effects of fat accumulation via a combination of catechins, EGCG, or caffeine were stronger collectively than by either catechins, EGCG, or caffeine alone. Moreover, it was demonstrated that the combination of catechins and caffeine induced inhibition of fat accumulation by suppression of fatty acid synthesis and upregulation of the enzymatic activities involved inβ-oxidation of fatty acid in the liver, but this result was not observed by combination of EGCG and caffeine.

scholarly journals Antcin K, a Triterpenoid Compound fromAntrodia camphorata, Displays Antidiabetic and Antihyperlipidemic Effects via Glucose Transporter 4 and AMP-Activated Protein Kinase Phosphorylation in Muscles

2016 ◽  
Vol 2016 ◽  
pp. 1-16 ◽  
Author(s):  
Yueh-Hsiung Kuo ◽  
Cheng-Hsiu Lin ◽  
Chun-Ching Shih ◽  
Chang-Syun Yang
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Protein Kinase ◽  
Total Cholesterol ◽  
Fatty Acid Synthase ◽  
Glucose Transporter ◽  
Control Group ◽  
Mrna Levels ◽  
Glucose Transporter 4 ◽  
Amp Activated Protein Kinase

The purpose of this study was to screen firstly the potential effects of antcin K (AnK), the main constituent of the fruiting body ofAntrodia camphorata,in vitroand further evaluate the activities and mechanisms in high-fat-diet- (HFD-) induced mice. Following 8-week HFD-induction, mice were treated with AnK, fenofibrate (Feno), metformin (Metf), or vehicle for 4 weeks afterward. In C2C12 myotube cells, the membrane GLUT4 and phospho-Akt expressions were higher in insulin and AnK-treated groups than in the control group. It was observed that AnK-treated mice significantly lowered blood glucose, triglyceride, total cholesterol, and leptin levels in AnK-treated groups. Of interest, AnK at 40 mg/kg/day dosage displayed both antihyperglycemic effect comparable to Metf (300 mg/kg/day) and antihypertriglyceridemic effect comparable to Feno (250 mg/kg/day). The combination of significantly increased skeletal muscular membrane expression levels of glucose transporter 4 (GLUT4) but decreased hepatic glucose-6-phosphatase (G6 Pase) mRNA levels by AnK thus contributed to a decrease in blood glucose levels. Furthermore, AnK enhanced phosphorylation of AMP-activated protein kinase (phospho-AMPK) expressions in the muscle and liver. Moreover, AnK treatment exhibited inhibition of hepatic fatty acid synthase (FAS) but enhancement of fatty acid oxidation peroxisome proliferator-activated receptorα(PPARα) expression coincident with reduced sterol response element binding protein-1c (SREBP-1c) mRNA levels in the liver may contribute to decreased plasma triglycerides, hepatic steatosis, and total cholesterol levels. The present findings indicate that AnK displays an advantageous therapeutic potential for the management of type 2 diabetes and hyperlipidemia.

scholarly journals Antidiabetic and Antihyperlipidemic Effects of Sulphurenic Acid, a Triterpenoid Compound from Antrodia camphorata, in Streptozotocin-Induced Diabetic Mice

2019 ◽  
Vol 20 (19) ◽  
pp. 4897 ◽  
Author(s):  
Cheng-Hsiu Lin ◽  
Li-Wei Hsiao ◽  
Yueh-Hsiung Kuo ◽  
Chun-Ching Shih
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Protective Effect ◽  
Fatty Acid Synthase ◽  
Control Group ◽  
Mrna Levels ◽  
Diabetic Mice ◽  
Antrodia Camphorata ◽  
Expression Levels ◽  
Lower Blood

The present study was designed to evaluate the protective effect of sulphurenic acid (SA), a pure compound from Antrodia camphorata, on diabetes and hyperlipidemia in an animal model study and to clarify the underlying molecular mechanism. Diabetes was induced by daily 55 mg/kg intraperitoneal injections of streptozotocin (STZ) solution over five days. Diabetic mice were randomly divided into six groups and orally gavaged with SA (at three dosages) or glibenclamide (Glib), fenofibrate (Feno) or vehicle for 3 weeks. Our findings showed that STZ-induced diabetic mice had significantly increased fasting blood glucose, glycated hemoglobin (HbA1C), plasma triglyceride (TG), and total cholesterol (TC) levels (p < 0.001, p < 0.001, p < 0.001, and p < 0.05, respectively) but decreased blood insulin, adiponectin, and leptin levels compared to those of the control group (p < 0.001, p < 0.001, and p < 0.001, respectively). Administration of SA to STZ-induced diabetic mice may lower blood glucose but it increased the insulin levels with restoration of the size of the islets of Langerhans cells, implying that SA protected against STZ-induced diabetic states within the pancreas. At the molecular level, SA treatment exerts an increase in skeletal muscle expression levels of membrane glucose transporter 4 (GLUT4) and phospho-Akt to increase the membrane glucose uptake, but the mRNA levels of PEPCK and G6Pase are decreased to inhibit hepatic glucose production, thus leading to its hypoglycemic effect. Moreover, SA may cause hypolipidemic effects not only by enhancing hepatic expression levels of peroxisome proliferator-activated receptor α (PPARα) with increased fatty acid oxidation but also by reducing lipogenic fatty acid synthase (FAS) as well as reducing mRNA levels of sterol regulatory element binding protein (SREBP)1C and SREBP2 to lower blood TG and TC levels. Our findings demonstrated that SA displayed a protective effect against type 1 diabetes and a hyperlipidemic state in STZ-induced diabetic mice.

scholarly journals Resveratrol attenuates steatosis in obese Zucker rats by decreasing fatty acid availability and reducing oxidative stress

2011 ◽  
Vol 107 (2) ◽  
pp. 202-210 ◽  
Author(s):  
S. Gómez-Zorita ◽  
A. Fernández-Quintela ◽  
M. T. Macarulla ◽  
L. Aguirre ◽  
E. Hijona ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Body Weight ◽  
Fatty Acid ◽  
Liver Disease ◽  
Fatty Acid Synthase ◽  
Liver Fat ◽  
Zucker Rats ◽  
Control Group ◽  
Acid Oxidation ◽  
Alcoholic Fatty Liver

Non-alcoholic fatty liver disease (NAFLD) is one of the most common manifestations of chronic liver disease worldwide. The aim of the present study was to assess the effect of resveratrol on liver fat accumulation, as well as on the activity of those enzymes involved in lipogenesis and fatty acid oxidation in fa/fa Zucker rats. A total of thirty rats were assigned to three experimental groups and orally treated with resveratrol for 6 weeks, or without resveratrol (C: control group; RSV15 group: 15 mg/kg body weight per d; RSV45 group: 45 mg/kg body weight per d). Liver histological analysis was performed by microscopy. Levels of hepatic carnitine palmitoyltransferase-Ia (CPT-Ia), acyl-coenzyme A oxidase (ACO), fatty acid synthase, glucose-6-phosphate dehydrogenase and malic enzyme were assessed by spectrophotometry, and acetyl-CoA carboxylase was assessed by radiometry. Commercial kits were used to determine serum TAG, NEFA, total HDL and non-HDL-cholesterol, glycerol, ketonic bodies, glucose, insulin, adiponectin, aspartate aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP), hepatic TAG, thiobarbituric acid reactive substrates, GSH (GSSG) and superoxide dismutase. Resveratrol reduced liver weight and TAG content. It did not modify the activity of lipogenic enzymes but it did increase CPT-Ia and ACO activities. NEFA and ALP were reduced in both resveratrol-treated groups. AST/GOT was reduced only by the lowest dose. ALT/GPT, TAG and adiponectin remained unchanged. Resveratrol reduced liver oxidative stress. This study demonstrates that resveratrol can protect the liver from NAFLD by reducing fatty acid availability. Moreover, resveratrol also protects liver from oxidative stress.

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