Fish oil and 3-thia fatty acid have additive effects on lipid metabolism but antagonistic effects on oxidative damage when fed to rats for 50 weeks

The 3-thia fatty acid tetradecylthioacetic acid (TTA) is a synthetic modified fatty acid, which, similar with dietary fish oil (FO), influences the regulation of lipid metabolism, the inflammatory response and redox status. This study was aimed to penetrate the difference in TTA's mode of action compared to FO in a long-term experiment (50 weeks of feeding). Male Wistar rats were fed a control, high-fat (25% w/v) diet or a high-fat diet supplemented with either TTA (0.375% w/v) or FO (10% w/v) or their combination. Plasma fatty acid composition, hepatic lipids and expression of relevant genes in the liver and biomarkers of oxidative damage to protein were assessed at the end point of the experiment. Both supplements given in combination demonstrated an additive effect on the decrease in plasma cholesterol levels. The FO diet alone led to removal of plasma cholesterol and a concurrent cholesterol accumulation in liver; however, with TTA cotreatment, the hepatic cholesterol level was significantly reduced. Dietary FO supplementation led to an increased oxidative damage, as seen by biomarkers of protein oxidation and lipoxidation. Tetradecylthioacetic acid administration reduced the levels of these biomarkers confirming its protective role against lipoxidation and protein oxidative damage. Our findings explore the lipid reducing effects of TTA and FO and demonstrate that these bioactive dietary compounds might act in a different manner. The experiment confirms the antioxidant capacity of TTA, showing an improvement in FO-induced oxidative stress.     

A Metabolomic Analysis of Two Intravenous Lipid Emulsions in a Murine Model

Background

Parenteral nutrition (PN), including intravenous lipid administration, is a life-saving therapy but can be complicated by cholestasis and liver disease. The administration of intravenous soy bean oil (SO) has been associated with the development of liver disease, while the administration of intravenous fish oil (FO) has been associated with the resolution of liver disease. The biochemical mechanism of this differential effect is unclear. This study compares SO and FO lipid emulsions in a murine model of hepatic steatosis, one of the first hits in PN-associated liver disease.

Methods

We established a murine model of hepatic steatosis in which liver injury is induced by orally feeding mice a PN solution. C57BL/6J mice were randomized to receive PN alone (a high carbohydrate diet (HCD)), PN plus intravenous FO (Omegaven®; Fresenius Kabi AG, Bad Homburg VDH, Germany), PN plus intravenous SO (Intralipid®; Fresenius Kabi AG, Bad Homburg v.d.H., Germany, for Baxter Healthcare, Deerfield, IL), or a chow diet. After 19 days, liver tissue was harvested from all animals and subjected to metabolomic profiling.

Results

The administration of an oral HCD without lipid induced profound hepatic steatosis. SO was associated with macro- and microvesicular hepatic steatosis, while FO largely prevented the development of steatosis. 321 detectable compounds were identified in the metabolomic analysis. HCD induced de novo fatty acid synthesis and oxidative stress. Both FO and SO relieved some of the metabolic shift towards de novo lipogenesis, but FO offered additional advantages in terms of lipid peroxidation and the generation of inflammatory precursors.

Conclusions

Improved lipid metabolism combined with reduced oxidative stress may explain the protective effect offered by intravenous FO in vivo.     

Effects of dietary fat energy restriction and fish oil feeding on hepatic metabolic abnormalities and insulin resistance in KK mice with high-fat diet-induced obesity

We investigated the effects of dietary fat energy restriction and fish oil intake on glucose and lipid metabolism in female KK mice with high-fat (HF) diet-induced obesity. Mice were fed a lard/safflower oil (LSO50) diet consisting of 50 energy% (en%) lard/safflower oil as the fat source for 12 weeks. Then, the mice were fed various fat energy restriction (25 en% fat) diets — LSO, FO2.5, FO12.5 or FO25 — containing 0, 2.5, 12.5, or 25 en% fish oil, respectively, for 9 weeks. Conversion from a HF diet to each fat energy restriction diet significantly decreased final body weights and visceral and subcutaneous fat mass in all fat energy restriction groups, regardless of fish oil contents. Hepatic triglyceride and cholesterol levels markedly decreased in the FO12.5 and FO25 groups, but not in the LSO group. Although plasma insulin levels did not differ among groups, the blood glucose areas under the curve in the oral glucose tolerance test were significantly lower in the FO12.5 and FO25 groups. Real-time polymerase chain reaction analysis showed fatty acid synthase mRNA levels significantly decreased in the FO25 group, and stearoyl-CoA desaturase 1 mRNA levels markedly decreased in the FO12.5 and FO25 groups. These results demonstrate that body weight gains were suppressed by dietary fat energy restriction even in KK mice with HF diet-induced obesity. We also suggested that the combination of fat energy restriction and fish oil feeding decreased fat droplets and ameliorated hepatic hypertrophy and insulin resistance with suppression of de novo lipogenesis in these mice.     

Fish oil and vitamin E supplementation in oxidative stress at rest and after physical exercise

Sen, Chandan K., Mustafa Atalay, Jyrki Ågren,David E. Laaksonen, Sashwati Roy, and Osmo Hänninen. Fishoil and vitamin E supplementation in oxidative stress at rest and afterphysical exercise. J. Appl. Physiol.83(1): 189-195, 1997.Fish oil supplementation and physicalexercise may induce oxidative stress. We tested the effects of 8 wk of-tocopherol (vitamin E) and fish oil (FO) supplementation on resting and exercise-induced oxidative stress. Rats(n = 80) were divided into groupssupplemented with FO, FO and vitamin E (FOVE), soy oil (SO), and SO andvitamin E (SOVE), and for FOVE and SOVE they were dividedinto corresponding exercise groups (FOVE-Ex and SOVE-Ex). Lipidperoxidation [thiobarbituric acid-reacting substances(TBARS)] was 33% higher in FO compared with SO in the liver, butoxidative protein damage (carbonyl levels) remained similar in bothliver and red gastrocnemius muscle (RG). Vitamin E supplementation,compared with FO and SO, markedly decreased liver and RG TBARS, butliver TBARS remained 32% higher in FOVE vs. SOVE. Vitamin E alsomarkedly decreased liver and RG protein carbonyl levels, althoughlevels in FOVE and SOVE were similar. Exercise increased liver and RGTBARS and RG protein carbonyl levels markedly, with similar levels inFOVE-Ex and SOVE-Ex. FO increased lipid peroxidation but not proteinoxidation in a tissue-specific manner. Vitamin E markedly decreasedlipid peroxidation and protein oxidation in both FOVE and SOVE,although liver lipid peroxidation remained higher in FOVE. Despitehigher levels of hepatic lipid peroxidation at rest in FOVE comparedwith SOVE, liver appeared to be relatively less susceptible toexercise-induced oxidative stress in FOVE.

     

High-protein diets prevent steatosis and induce hepatic accumulation of monomethyl branched-chain fatty acids

The hallmark of nonalcoholic fatty liver disease is steatosis of unknown etiology. To test how dietary protein decreases steatosis, we fed female C57BL/6 J mice low-fat (8 en%) or high-fat (42 en%) combined with low-protein (11 en%), high-protein (HP; 35 en%) or extra-high-protein (HPX; 58 en%) diets for 3 weeks. The 35 en% protein diets reduced hepatic triglyceride, free fatty acid, cholesterol and phospholipid contents to ~50% of that in 11 en% protein diets. Every additional 10 en% protein reduced hepatic fat content ~1.5 g%. HP diets had no effect on lipogenic or fatty acid-oxidizing genes except Ppargc1α (+30%), increased hepatic PCK1 content 3- to 5-fold, left plasma glucose and hepatic glycogen concentration unchanged, and decreased inflammation and cell stress (decreased Fgf21 and increased Gsta expression). The HP-mediated decrease in steatosis correlated inversely with plasma branched-chain amino-acid (BCAA) concentrations and hepatic content of BCAA-derived monomethyl branched-chain fatty acids (mmBCFAs) 14-methylpentadecanoic (14-MPDA; valine-derived) and, to a lesser extent, 14-methylhexadecanoic acid (isoleucine-derived). Liver lipid content was 1.6- to 1.8-fold higher in females than in males, but the anti-steatotic effect of HP diets was equally strong. The strong up-regulation of PCK1 and literature data showing an increase in phosphoenolpyruvate and a decline in tricarboxylic acid cycle intermediates in liver reveal that an increased efflux of these intermediates from mitochondria represents an important effect of an HP diet. The HP diet-induced increase in 14-MPDA and the dietary response in gene expression were more pronounced in females than males. Our findings are compatible with a facilitating role of valine-derived mmBCFAs in the antisteatotic effect of HP diets.     

Growth performance,fatty‐acid composition,lipid deposition and hepatic‐lipid metabolism‐related gene expression in juvenile pond loach Misgurnus anguillicaudatus fed diets with different dietary soybean oil levels

A 10 week feeding trial was conducted to evaluate the effects of different dietary soybean oil (SO) levels on growth performance, fatty‐acid composition and lipid deposition in viscera, histology and histochemistry of liver, intestine and hepatic‐lipid metabolism‐related gene expressions in pond loach Misgurnus anguillicaudatus juveniles. Misgurnus anguillicaudatus (mean ± s.d. mass 0·40 ± 0·01 g) were fed five experimental diets containing SO at different concentrations: 0, 20, 32, 56 and 100% SO and a diet containing 100% fish oil (100% FO). The mass gains and specific growth rates of M. anguillicaudatus fed 20% SO and 100% FO diets were significantly higher than those of the other groups (P < 0·05). The lipid content of viscera and the amount of cytoplasmic vacuolation in the liver increased with incremental dietary SO level. Meanwhile, increasing dietary SO levels up‐regulated the messenger (m)RNA levels of lipogenic genes (such as Δ6fad, scd, pparγ, fas and srebp‐1) and down‐regulated the mRNA levels of the lipolytic genes (such as pparα, cpt1, atgl and hsl) in the liver. The percentage of 20:4n‐6 significantly (P < 0·05) increased with increasing dietary SO level, which might be correlated with the up‐regulation of the mRNA level of Δ6fad. The highest levels of dietary SO, however, had a negative effect on growth performance, lipid deposition of viscera and histology and histochemstry of liver and intestine. The increased lipid accumulation induced by incremental dietary SO level probably occurred through different strategies for lipid metabolism as a result of competition between lipolysis and lipogenesis and between export and import of lipids in this species.     

不同脂肪源对泥鳅稚鱼生长性能及脂肪酸组成的影响

为研究饲料不同脂肪源对泥鳅稚鱼生长性能及鱼体脂肪酸组成的影响, 实验选择初始体重为(10.002.00) mg的健康泥鳅稚鱼1500尾, 随机分为5组, 每组3个重复, 每个水箱100尾鱼, 分别投喂5种含有鱼油(FO)、大豆油(SO)、玉米油(CO)、花生油(PeO)和棕榈油(PaO)的配合饲料, 每种饲料3个重复, 饲养期为40d。结果显示, 摄食不同脂肪源饲料的泥鳅稚鱼在增重率、成活率、饲料系数等生长性能指标和体成分上没有显著差异(P0.05), 但是, 摄食FO组鱼体极性脂肪含量显著高于其他植物油组(P0.05)。鱼油组鱼体中性和极性脂肪中总n-3系脂肪酸含量和EPA+DHA含量显著高于其他植物油组(P0.05)。植物油组鱼体极性脂肪中20:4n-6含量显著高于鱼油组(P0.05), 表明泥鳅稚鱼具有将C18转换为C20的能力。研究表明, 在饲料中添加足量磷脂, 鱼油、大豆油、玉米油、花生油、棕榈油都可以用作泥鳅稚鱼期专用饲料脂肪源。     

再投喂鱼油对瓦氏黄颡鱼肌肉脂肪酸组成的影响

为研究植物油替代鱼油对瓦氏黄颡鱼（Pelteobagrus vachelli）生长及肌肉脂肪组成的影响及重投喂鱼油对瓦氏黄颡鱼肌肉脂肪酸组成的影响,实验以大豆油分别替代饲料中的0（FO）、50（S1）、75（S2）和100%（SO）的鱼油配制等氮、等能的颗粒饲料,每组设置3个平行,养殖80d后,再投喂鱼油30d。结果表明,饲料中添加豆油不会显著影响瓦氏黄颡鱼的增重率、肝体指数和体成分（P>0.05）。随着饲料中大豆油含量的增加,S2和SO组肌肉中C18:1n-9、C18:2n-6和单不饱和脂肪酸比例显著增加（P < 0.05）,而C20:5n-3,C22:5n-3及n-3/n-6比例显著下降（P < 0.05）。再投喂鱼油30d后,SO组肌肉中C18:3n-6、C20:4n-6、Σ n-9、Σ n-6和S2组中C18:1n-9、Σ n-6比例显著下降（P < 0.05）,而S2和SO组肌肉中Σn-3多不饱和脂肪酸、C20:5n-3和C22:5n-3比例显著增加（P < 0.05）。在生产中,可采用先植物油饲料、后鱼油饲料的养殖方式提高瓦氏黄颡鱼肌肉品质（增加有益人类健康的多不饱和脂肪酸）。     

The Fat-1 Mouse has Brain Docosahexaenoic Acid Levels Achievable Through Fish Oil Feeding

Fat-1 transgenic mice endogenously convert n-6 to n-3 polyunsaturated fatty acids (PUFA). The aims of this study were to test whether a) fish oil feeding can attain similar brain n-3 PUFA levels as the fat-1 mouse, and b) fat-1 mouse brain docosahexaenoic acid (22:6n-3; DHA) levels can be potentiated by fish oil feeding. Fat-1 mice and their wildtype littermates consumed either a 10% safflower oil (SO) or a 2% fish oil and 8% safflower oil chow (FO). Brain total lipid and phospholipid fraction fatty acids were analyzed using GC-FID. Wildtype mice fed FO chow had similar brain levels of DHA as fat-1 mice fed SO chow. Fat-1 mice fed FO chow had similar brain n-3 PUFA levels as fat-1 mice fed SO chow. In conclusion, brain levels of DHA in the fat-1 mouse can be obtained by and were not further augmented with fish oil feeding.     

Suppression of oxidative stress in aging NZB/NZW mice: effect of fish oil feeding on hepatic antioxidant status and guanidino compounds

Oxidative stress caused by excessive reactive species (RS) and lipid peroxidation is known to be casually linked to age-related inflammation. To test the hypothesis that fish oil (FO) intake has a beneficial effect on nephritis due to its suppressive action of oxidative stress and the enhancement of antioxidant defenses, we examined the effect of dietary FO on various oxidative stress-related parameters and guanidino compound (GC) levels using (NZB × NZW) F₁ (B/W) mice. These mice were fed diets supplemented with either 5% corn oil (control) or 5% FO. At 4 and 9 months of age, the hepatic oxidative status was estimated by assessing RS generation produced from xanthine oxidase, the prostaglandin pathway and lipid peroxidation. To evaluate the effect of FO on redox status, including antioxidant defenses, GSH and GSSG levels and antioxidant enzyme activities were measured. To correlate the extent of oxidative status with the nephritic condition, creatinine, guanidino acetic acid and arginine levels were measured. Results indicated that increased levels of lipid peroxidation, RS generation and xanthine oxidase activity with age were all significantly suppressed by FO feeding. Furthermore, reduced GSH levels, GSH/GSSG ratio and antioxidant enzyme activities in the FO-fed mice were effectively enhanced compared to the corn oil-fed mice. Among several GCs, the age-related increase of creatinine level was blunted by FO. Based on these results, we propose that dietary FO exerts beneficial effects in aged, nephritic mice by suppressing RS, superoxide and lipid peroxidation, and by maintaining a higher GSH/GSSG ratio and antioxidant enzyme activities.     

Cold storage effects on flesh quality of rainbow trout Oncorhynchus mykiss (Walbaum, 1792) fed diets containing different vegetable oils

The intention of this experiment was to assess the effects of different sources of dietary lipid on the fatty acid composition of the fillet and liver and the flesh quality traits of rainbow trout (Oncorhynchus mykiss) after a 70‐day feeding period. Four iso‐nitrogenous (approx. 51% crude protein) and iso‐lipidic (approx. 14% crude lipid) experimental diets were formulated. The control diet contained only fish oil (FO) as the primary lipid source. In the other three dietary treatments, fish oil was replaced by 100% (LO30/SO35/SFO35) and 70% (FO30/LO35/SO35 or FO30/SO35/SFO35) sesame oil (SO), linseed oil (LO), or sunflower oil (SFO). Triplicate groups of 40 rainbow trout (~46 g) held under similar culture conditions were hand‐fed daily to apparent satiation for 70 days. At the end of the feeding trials, no difference in growth performance among experimental groups was noted (P > 0.05). There were some differences in the proximate composition of fish fillets (P < 0.05): the eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) levels were highest in fish fed the control diet (P < 0.05); and EPA and DHA levels in fish fed the FO30/LO35/SO35 diet were closest to the control diet (P < 0.05). In contrast, fish fed the diet containing 100% plant oils (LO30/SO35/SFO35) had the highest level of total n‐6 fatty acids in the fillet and liver. In a 12‐day refrigerated storage at 1°C the thiobarbituric acid (TBA), trimethylamin nitrogen (TMA‐N) and pH values gradually increased in all dietary groups (P < 0.05). The chemical indicators of spoilage, TBA, TMA‐N, and pH values were within the limit of acceptability for human consumption.     

不同脂肪源对异育银鲫的生长、体组成和肌肉脂肪酸的影响

配制了十种等氮等能的饲料饲喂3.53 g的异育银鲫幼鱼12周, 探讨异育银鲫对不同脂肪源的利用效果。十种饲料中分别添加8%的鱼油(FO)、椰子油(CNO)、玉米油(CO)、亚麻油(LO)、大豆油(SO)、菜籽油(RO)、1∶1鱼油-椰子油(FCNO)、1∶1鱼油-玉米油(FCO)、1∶1鱼油-亚麻油(FLO)和1∶1∶1∶1鱼油-椰子油-玉米油-亚麻油混合油(MIX)。每组饲料三个平行, 每个平行30尾。实验在循环水养殖系统中进行, 水温控制在(241)℃。结果表明, 在单一脂肪源中, 豆油组和椰子油组的增重率最高, 其次是菜籽油组, 鱼油、玉米油和亚麻油组的增重率最低。与相应的单一脂肪源相比, 饲料中鱼油与椰子油、玉米油或亚麻油1∶1混合后使用提高了异育银鲫的生长。摄食不同脂肪源饲料的异育银鲫血清生化指标、各组织的水分和脂肪含量差异不明显(P0.05)。肌肉脂肪酸与饲料脂肪源呈明显正相关。摄食豆油和菜籽油饲料的鱼体肌肉中20:4n-6较高, 而摄食亚麻油饲料的鱼则含有较高的20:5n-3和22:6n-3, 表明异育银鲫具有转化18:2n-6和 18:3n-3为高不饱和脂肪酸的能力。从实验可以看出, 豆油、椰子油和菜籽油是异育银鲫饲料中良好的脂肪源。       

蚕蛹基础日粮中添加不同脂肪源对框鳞镜鲤生长、体成分及健康状况的影响

将324尾健康框鳞镜鲤Cyprinus carpio var. specularis (10.700.70) g随机平均分配在室内循环水养殖系统的12个养殖缸里。在蚕蛹基础饲料中分别添加2%的大豆油(SO)、菜籽油(RO)、鱼油(FO)及混合油(MIX, 大豆油:菜籽油:鱼油=1:1:1), 配制4组等氮(36.5%)等脂(7.0%)饲料, 饲养58d后, 探讨框鳞镜鲤对不同脂肪源的利用效果。结果表明:(1)大豆油组终末体重显著大于混和油组, 肠长比显著大于其他各组, 肥满度和肠指数显著大于鱼油组(P0.05); 肝胰脏指数混合油组显著低于鱼油组和大豆油组, 菜籽油组显著低于大豆油组(P0.05); (2)全鱼水分大豆油组显著高于菜籽油组和混合油组, 粗脂肪含量显著低于其他各组(P0.05); 肌肉水分大豆油组显著大于鱼油组和混合油组(P0.05); 不同脂肪源对框鲤全鱼和肌肉的粗蛋白和灰分、肌肉粗脂肪、肝胰脏的一般体成分无显著影响(P0.05); (3)肝胰脏和肌肉脂肪酸组成基本反映了饲料的脂肪酸组成; 肝胰脏PUFA水平大豆油和菜籽油组相近, 均显著高于鱼油组(P0.05); 肌肉PUFA水平大豆油组显著高于鱼油组(P0.05), 肌肉HUFA水平菜籽油组显著高于鱼油组和混合油组(P0.05); (4)除菜籽油组血清GLU水平显著高于大豆油组外(P0.05), 4种脂肪源对框鲤其他血清生化指标水平没有显著影响(P0.05); (5)组间血清T-SOD活性没有显著差异(P0.05), 大豆油组GSH-XP活性显著大于其他各组(P0.05), MDA水平显著低于鱼油组及混合油组(P0.05), 鱼油组血清AKP活性显著低于其他各组(P0.05); 鱼油组肝胰脏T-SOD活性显著高于其他各组(P0.05), AKP活性显著高于菜籽油组和混合油(P0.05), GSH-XP活性显著高于混合油组(P0.05), MDA水平各组无显著差异(P0.05)。综上所述, 框鳞镜鲤对大豆油的利用效果最好, 其次是菜籽油、鱼油和混合油利用效果较差。       

Increased n-3 polyunsaturated fatty acid content of red blood cells from fish oil-fed rabbits increases in vitro lipid peroxidation, but decreases hemolysis.

In view of a possible relationship between fish oil, lipid peroxidation, and atherosclerosis, the in vitro lipid peroxidation susceptibility of red blood cells (RBCs) from rabbits on conventional (-FO) and fish oil-enriched diets (+FO) was investigated. The diet caused substantial increases in the RBC concentrations of n-3 polyunsaturated fatty acids (PUFAs), in combination with decreases in the concentration of oleic acid (18:1) and linoleic acid (18:2). Cumene hydroperoxide-induced oxidative stress led to increased overall fatty acid peroxidation in +FO RBCs compared with with -FO RBCs, as quantitated by GLC fatty acid analysis. However, the increased overall susceptibility to lipid peroxidation of +FO RBCs was not reflected in increased peroxidation of every individual fatty acid. This was observed for endogenous arachidonic acid (20:4) as well as, in separate experiments, for exogenously added parinaric acid (PnA). The increased cumene hydroperoxide-induced PUFA oxidation in +FO RBCs was accompanied by a lesser extent of hemolysis. To account for these observations, it is proposed that the increased n-3 PUFA content of +FO RBCs serves as an oxidizable buffer. The present data suggest that oxidation of fatty acids can occur until a critically low level of intact phospholipid in the RBC membrane is reached, after which the membrane destabilizes and hemolysis occurs. At the same time, the PUFA buffer in +FO RBCs could also prevent oxidative damage to specific membrane proteins, which could also help prevent cell lysis.     

Alterations of gene expression profiles induced by sulfur dioxide in rat lungs

Sulfur dioxide (SO2) is a ubiquitous air pollutant presents in low concentrations in urban air and in higher concentrations in working environment.Few data are avail-able on the effects of being exposed to this pollutant on the molecular mechanism,although some biochemical changes in lipid metabolism,intermediary metabolism and oxidative stress have been detected.The present investigation aimed at analyzing the gene expression profiles of the lungs of Wistar rats short-term (20 ppm,6 h/day,for seven days) and long.term (5 ppm,1 h/day,for 30 days) exposed to SO2 by Affymetrix GeneChip (RAE230A) analysis.It was found that 31 genes,containing 18 known genes and 13 novel genes were up-regulated,and 31 genes,containing 20 known genes and 11 novel genes,were down-regulated in rats short-term exposed to SO2 compared with control rats.While there were 176 genes,containing 82 known genes and 94 novel genes were up-regulated,and 85 genes,containing 46 known genes and 39 novel genes,were down-regulated in rats long-term exposed to SO2 compared with control rats.It is suggested that:(1) SO2 exerts its effects by different mechanisms in vivo at high-dose short-term inhalation and at low-dose long-term inhalation;(2) a notable feature of the gene expression profile was the decreased expression of genes related to oxidative phosphorylation in lungs of rats short-term exposed to SO2,which shows high-dose short-term exposed to SO2 may cause the deterioration of mitochondrial functions;(3)discriminating genes in lungs of rats long-term exposed to SO2 included those involved in fatty acid metabolism,immune,inflammatory,oxidative stress,oncogene,tumor suppresser and extracellular matrix.The mechanism of low-dose long-term exposed to SO2 is more complex.     

Tremella fuciformis Crude Polysaccharides Attenuates Steatosis and Suppresses Inflammation in Diet-Induced NAFLD Mice

Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disorder characterized by an enhanced accumulation of lipids, which affects around 40% of the world’s population. The T. fuciformis fungus possesses immunomodulatory activity and other beneficial properties that may alleviate steatosis through a different mechanism. The present study was designed to evaluate the effect T. fuciformis crude polysaccharides (TFCP) on inflammatory and lipid metabolism gene expression, oxidative stress, and lipid profile. Mice were divided into groups receiving (a) a normal chow diet (NCD), (b) a methionine–choline-deficient (MCD) diet, and (c) a MCD diet with TFCP. Liver histopathology was performed, and the hepatic gene expression levels were estimated using qRT-PCR. The lipid profiles, ALT, AST, and efficient oxidative enzymes were analyzed using ELISA. The TFCP administration in the MCD-fed mice suppressed hepatic lipid accumulation, lipid metabolism-associated genes (HMGCR, FABP, SREBP, ACC, and FAS), and inflammation-associated genes (IL-1β, TLR4, TNF-α, and IL-6) whilst enhancing the expression of HNF4α genes. TFCP mitigated against oxidative stress and normalized healthy lipid profiles. These results highlighted that TFCP prevents NAFLD through the inhibition of oxidative stress and inflammation, suggesting TFCP would potentially be an effective therapeutic agent against NAFLD progression.     

Dietary β-conglycinin prevents fatty liver induced by a high-fat diet by a decrease in peroxisome proliferator-activated receptor γ2 protein

Diets high in sucrose/fructose or fat can result in hepatic steatosis (fatty liver). Mice fed a high-fat diet, especially that of saturated-fat-rich oil, develop fatty liver with an increase in peroxisome proliferator-activated receptor (PPAR) γ2 protein in liver. The fatty liver induced by a high-fat diet is improved by knockdown of liver PPARγ2. In this study, we investigated whether β-conglycinin (a major protein of soy protein) could reduce PPARγ2 protein and prevent high-fat-diet-induced fatty liver in ddY mice. Mice were fed a high-starch diet (70 energy% [en%] starch) plus 20% (wt/wt) sucrose in their drinking water or a high-safflower-oil diet (60 en%) or a high-butter diet (60 en%) for 11 weeks, by which fatty liver is developed. As a control, mice were fed a high-starch diet with drinking water. Either β-conglycinin or casein (control) was given as dietary protein. β-Conglycinin supplementation completely prevented fatty liver induced by each type of diet, along with a reduction in adipose tissue weight. β-Conglycinin decreased sterol regulatory element-binding protein (SREBP)-1c and carbohydrate response element-binding protein (ChREBP) messenger RNAs (mRNAs) in sucrose-supplemented mice, whereas it decreased PPARγ2 mRNA (and its target genes CD36 and FSP27), but did not decrease SREBP-1c and ChREBP mRNAs, in mice fed a high-fat diet. β-Conglycinin decreased PPARγ2 protein and liver triglyceride (TG) concentration in a dose-dependent manner in mice fed a high-butter diet; a significant decrease in liver TG concentration was observed at a concentration of 15 en%. In conclusion, β-conglycinin effectively prevents fatty liver induced by a high-fat diet through a decrease in liver PPARγ2 protein.     

Dietary fatty acid composition affects the repeat swimming performance of Atlantic salmon in seawater

Repeated critical swimming performance trials (Ucrit) were performed on Atlantic salmon (Salmo salar) to test the null hypothesis that the source of dietary lipids (fish-based, poultry-based, and plant-based) does not influence exercise and recovery performance. Four diets were prepared by extensively replacing supplemental lipid from anchovy oil (AO; 100% AO at 150 g/kg) with cold pressed flaxseed oil (FO; 25% AO, 75% FO), sunflower oil (SO; 25% AO, 75% SO), or poultry fat (PF; 25% AO, 75% PF). These diets had equivalent protein and energy concentrations, but due to the different supplemental lipid sources, varied widely in their fatty acid composition. Fish fed AO had a significantly higher (P<0.05) first Ucrit (2.62+/-0.07 body lenght s(-1)) than those fed PF (2.22+/-0.12 body lenght s(-1)) that had low muscle ratios of n-3 highly unsaturated fatty acids (n-3 HUFA) to saturated fatty acids (SFA) and arachidonic acid (AA), and high levels of oleic acid. Fish in the FO and SO diet groups swam as well as AO-fed fish in both swimming trials. The performance of fish fed AO decreased significantly (P<0.05) during the second swimming trial (i.e. Ucrit2/Ucrit1=0.92+/-0.02). No significant differences occurred between diet groups for the second swim trial. There was a positive correlation between both n-3 HUFA/SFA and n-3 HUFA/AA ratios, and Ucrit1. A negative correlation was found between dietary AA and oleic acids, and Ucrit1. The present study suggests that low dietary n-3 HUFA/ SFA and n-3 HUFA/AA ratios may negatively affect swimming performance. The former possibly can be offset by increasing linoleic acid in the presence of nutritionally adequate n-3 HUFA (e.g. SO diet). Lipid supplements consisting largely of vegetable oils did not compromise fish cardiorespiratory physiology under the conditions of this study.