Goose fatty liver is one of the most delicious and popular foods in the world, but there is no reliable genetic marker for the early selection and breeding of geese with good liver-producing potential. In our study, one hundred and twenty-four 78-day-old Landes geese bred in Shunda Landes goose breeding farm, Jiutai, Jilin, China were selected randomly. The fatty livers were sampled each week after overfeeding during a three week period. Polymerase chain reaction-single strand conformation polymorphism and DNA sequencing were used to identify single nucleotide polymorphisms (SNPs) of fatty acid synthase (FAS), which is an important enzyme involved in the synthesis of fat under both physiological and pathological conditions. Least-squares correlation was established between these SNPs and fatty liver weight, abdominal fat weight, and intestinal fat weight of the overfed Landes geese, respectively. The results showed that fatty liver weight of geese with EF and FF genotypes (amplified by primer P1) was significantly higher than that of the EE genotype (p<0.05), and liver weight of CD and DD genotypes (amplified by primer P2) was significantly higher than that of the CC genotype (p<0.05). Different genotype combinations showed different liver weights, and from highest to lowest were ABDD, DDEF, DDFF, DDEE, ABEF, ABFF, AADD, and CDEF. Further analysis of DNA sequencing showed that there were two SNPs within the 5' promoter region the FAS gene. The geese of EF and FF genotypes carried a change of T to C, and the geese of CD and DD genotypes carried a change of A to G. The changes of the bases could potentially influence the binding of some transcription factors to this region as to regulate FAS gene. To our knowledge, this is the first report of SNPs found within the 5' promoter region of the Landes goose FAS gene, and our data will provide an insight for early selection of geese for liver production.
Objectives : This study was undertaken to investigate the effects of the GGEx18 ethyl acetate fraction (EF) on lipid accumulation and gene expression of fatty acid-oxidizing enzymes using 3T3-L1 adipocytes, C2C12 skeletal muscle cells, and NMu2Li liver cells. Methods : PPAR${\alpha}$, AMPK and UCPs transactivation was examined in NMu2Li hepatocytes, C2C12 myocytes, and 3T3-L1 preadipocytes using transient transfection assays. Results : 1. Compared with control, EF significantly increased the mRNA expression of VLCAD in 3T3-L1 adipocytes. 2. Compared with control, EF (0.1 ${\mu}g/ml$) significantly inhibited lipid accumulation in 3T3-L1 adipocytes. 3. EF significantly increased the mRNA expression of AMPK${\alpha}$1, AMPK${\alpha}$2 and PPAR${\alpha}$ in C2C12 skeletal muscle cells compared with control. 4. EF significantly increased the mRNA expression of genes involved in fatty acid ${\beta}$-oxidation, such as thiolase, MCAD, and CPT-1 in C2C12 skeletal muscle cells compared with control. 5. EF significantly increased the mRNA expression of UCP2 involved in energy expenditure in C2C12 skeletal muscle cells compared with control. 6. Compared with control, EF (10 ${\mu}g/ml$) significantly inhibited lipid accumulation in C2C12 skeletal muscle cells. 7. EF (10 ${\mu}g/ml$) significantly increased the mRNA expression of ACOX, HD, VLCAD and MCAD in NMu2Li liver cells compared with control. Conclusions : These results suggest that EF may prevent obesity by increasing the mRNA expression of mitochondrial fatty acid ${\beta}$-oxidizing enzymes in 3T3-L1 adipocytes, by not only regulating the fatty acid oxidation through activation of AMPK and PPAR${\alpha}$, but also increasing the UCP2 mRNA expression in C2C12 skeletal muscle cells, and by stimulating the mRNA expression of fatty acid-oxidizing enzymes in NMu2Li liver cells.
This study investigated the effects of cod liver oil and chromium picolinate on the serum traits and egg yolk fatty acids and cholesterol content in laying hens. One hundred 45-week old single comb white Leghorn laying hens were assigned randomly to four groups. These groups were: (1) control (soybean oil), (2) 1,000 ppb (${\mu}g/kg$) chromium (organic form chromium picolinate) (Crpic), (3) 3% cod liver oil (CLO), and (4) 1,000 ppb chromium with 3% cod liver oil (CLO+Crpic). The experiment was conducted for 40 days. Results indicated that serum triacylglycerol (TG) and cholesterol contents in the CLO group and the serum glucose content in the Crpic group were significantly lower than those in the control group (p<0.05-0.01). The yolk cholesterol content in the CLO and Crpic groups were also lower than the control group (p<0.01). The lipoprotein profile displayed that in the Crpic group, high-density lipoprotein (HDL) and HDL-cholesterol (HDL-C) were significantly higher (P<0.05) than the control group. Meanwhile, low-density lipoprotein+very low-density lipoprotein (LDL+VLDL) and LDL-C+VLDL-C were significantly lower (p<0.05) than the control group. Notably, of all four groups, the CLO group displayed a more profound effect on serum traits and lipoprotein (p<0.05-0.001). Furthermore, the fatty acid composition of the egg yolks presented that C18:2 in the CLO and Crpic groups was significantly lower (p<0.05-0.001) compare to the control. However, only in the CLO group, C18:3, C20:5 and C22:6 were significantly higher (p<0.001) than the control. Only serum glucose and LDL+VLDL showed the CLO${\times}$Crpic interaction (p<0.05), most parameters did not. Therefore, supplemented chromium picolinate or cod liver oil in the diet of laying hens had beneficial effects. However, when these two factors were combined, there was no interaction with most parameters.
Kim, Yu Gon;Kim, Jae Hyeon;Jo, Yong Wan;Kwun, Min Jung;Han, Chang Woo
대한한의학회지
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제36권4호
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pp.74-79
/
2015
Objectives: Here we investigated the anti-lipogenic potential of kaurenoic acid (KA), a diterpene derived from Aralia continentalis, in a cellular model of non-alcoholic fatty liver disease. Methods: HepG2 cells were treated with palmitate for 24h to induce intracellular lipid accumulation. To assess the influence of KA on steatotic HepG2 cells, various concentration of KA was co-administered. After palmitate treatment, Intracellular triglyceride content was measured. Expression level of several lipogenic genes, sterol regulatory element-binding transcription factor-1c (SREBP-1c), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), and stearoyl-CoA desaturase-1 (SCD-1) were measured using Western-blot analyses or RT-PCR. Results: Palmitate markedly increased intracellular triglyceride level and expression of related lipogenic genes in HepG2 cells, and which was relieved by co-administered KA. Conclusions: It is conceivable that that KA may have a pharmacological potential to reduce lipid accumulation in non-alcoholic fatty liver disease.
This study was carried out to investigate the effect of the feeding mixture of linesed oil, rich in n-3 PUFA and the sunflower seed oil, rich in n-6 PUFA on the lipid metabolism in the dietary hypprlidemic rats. After male Sprague-Dawley rats were induced hyperlipidemia by feeding the diet containing lard, butter, and cholesterol for 3 weeks, then they were fed with the diet containing lard 3.0% and butter 12.0% for control, the mixture in different proportion of both linseed oil and sunflower seed oil, and antihyperlipidemic durgs for 2 weeks. Analysis of the lipid component and the fatty acid composition of the liver showed following results. Concentration s of the total cholesterol and phospholipid in liver were significantly higher in group 2 (olive oil 12.0%) and lower in the other groups than in the control group, especially lower in groups 3 (cholestyramine 2.0%) and 9 (sunflower seed oil 12.0%) . Concentration of triglyceride was lower in the other groups except group 4 (liparoid), especially lowe rin group 9 than in the control group. In the fatty acid composition of liver lipids, C18:2 was the major fatty acid. Contents of n-6 PUFA increased , while those of n-3 PUFA decreased in groups composition of the test lipids. From the data on concentration s of total cholesterol. Phospholipid and triglyceride in liver, we concluded that the feeding mixed with 3.0% lard and 12.0 % sunflower seed oil were most effective for the improvement of the live lipids. The fatty acid composition in liver lipids were affected by the fatty acid composition of the test lipids.
Purpose: Due to the increasing prevalence of obesity worldwide, non-alcoholic fatty liver disease (NAFLD) has reached epidemic dimensions over time. NAFLD is the most common cause of childhood chronic liver disease. There is a relationship between NAFLD and oxidative stress. This study aims to investigate the changes in thiol/disulfide homeostasis parameters to determine the oxidant/antioxidant balance in obese rats with diet-induced NAFLD and healthy rats. Methods: Twelve Wistar albino rats were used in this study. Experimentally produced NAFLD obese rats (n=6) and healthy rats were compared. Experimental NAFLD model was created with a special fatty liver diet (Altromin® C1063, Fatty Liver Diet, Exclusivet, Lage, Germany). The biochemical and histopathological features of the groups, as well as serum thiol/disulfide homeostasis parameters, were analyzed and compared. Results: In the experimentally induced NAFLD rat model, they gained more weight than the control group. Steatosis (at least grade 2) occurred in all rats fed with special fatty liver diet for 12 weeks. Histopathologically, no high-grade inflammation was observed in rats with experimental NAFLD after feeding a diet for 12 weeks. Results revealed that aspartate transaminase and alanine transaminase levels were high, albumin levels were low, oxidant stress parameters increased, and antioxidant thiol groups decreased. Conclusion: Experimental NAFLD is characterized by increased oxidant stress accompanying fatty tissue in the liver. Analysis of thiol/disulfide homeostasis parameters in NAFLD can be used in further studies to develop effective treatment options.
Cardiovascular diseases (CVDs) are the most common cause of death in patients with nonalcoholic fatty liver disease (NAFLD) and dyslipidemia is considered at least partially responsible for the increased CVD risk in NAFLD patients. The aim of the present study is to understand how hepatic de novo lipogenesis influences hepatic cholesterol content as well as its effects on the plasma lipid levels. Hepatic lipogenesis was induced in mice by feeding a fat-free/high-sucrose (FF/HS) diet and the metabolic pathways associated with cholesterol were then analyzed. Both liver triglyceride and cholesterol contents were significantly increased in mice fed an FF/HS diet. Activation of fatty acid synthesis driven by the activation of sterol regulatory element binding protein (SREBP)-1c resulted in the increased liver triglycerides. The augmented cholesterol content in the liver could not be explained by an increased cholesterol synthesis, which was decreased by the FF/HS diet. HMG-CoA reductase protein level was decreased in mice fed an FF/HS diet. We found that the liver retained more cholesterol through a reduced excretion of bile acids, a reduced fecal cholesterol excretion, and an increased cholesterol uptake from plasma lipoproteins. Very low-density lipoproteintriglyceride and -cholesterol secretion were increased in mice fed an FF/HS diet, which led to hypertriglyceridemia and hypercholesterolemia in Ldlr-/- mice, a model that exhibits a more human like lipoprotein profile. These findings suggest that dietary cholesterol intake and cholesterol synthesis rates cannot only explain the hypercholesterolemia associated with NAFLD, and that the control of fatty acid synthesis should be considered for the management of dyslipidemia.
The nutritional contribution of mideodeok extracts (ME) on rockfish (Sebastes schlegelii) feed and fish muscle was investigated. Different concentrations of the ME mixed with commercial diet were fed to mature rockfish for 8 weeks. The lipid and ash contents of the formulated diets were relatively similar to the control diet, while increasing the extract concentration increased the moisture content and decreased the protein contents. Major fatty acid components (C18:1n-9, 16:0, C20:5n-3, C22:6n-3) were of comparable quantity. High presence of C18:2n-6 was attributed to soybean oil incorporated in the diets, while the essential fatty acids were within limits (0.9-1.0%). The diet fortified with 6% ME produced the highest feed efficiency, with increased protein content in the muscle as well as lipid content for both muscle and liver. Hepato- and visceral-somatic index values were elevated with increasing ME concentration Muscle fatty acid contents were mostly C18:1n-9 and C16:0, with low absorption of C18:2n-6 in both the muscle and liver. Total highly unsaturated fatty acid content was significantly reduced in the fish muscle, but the values were higher for fish fed with a ME-fortified diet. An increasing trend for eicosapentaenoic acid and docosahexaenoic acid was also observed with increased ME fortification, with liver levels of these compounds remaining within range throughout the duration of the experiment.
Objectives : We tried to uncover the anti-lipogenic effect and underlying mechanism of Laminaria japonica on an experimental cellular model of non-alcoholic fatty liver disease. Methods : Ethanol extract of Laminaria japonica (LJ) was prepared. Intracellular lipid content of palmitate-treated HepG2 cells was evaluated with or without LJ treatment. We measured the effects of LJ on liver X receptor ${\alpha}$ ($LXR{\alpha}$) and sterol regulatory element-binding transcription factor-1c (SREBP-1c) expression, transcription level of lipogenic genes, including acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS), stearoyl-CoA desaturase-1 (SCD-1), and nuclear factor erythroid 2-related factor 2 (Nrf2) activation in HepG2 cells. Results : LJ markedly attenuated palmitate-induced intracellular lipid accumulation in HepG2 cells. LJ suppressed $LXR{\alpha}$-dependent SREBP-1c activation, and SREBP-1c mediated induction of ACC, FAS, and SCD-1. Furthermore, LJ activated Nrf2, which plays an important cytoprotective role in non-alcoholic fatty liver disease. Conclusions : Our study suggests that LJ has the potential to alleviate hepatic lipid accumulation, and this effect was mediated by inhibiting the $LXR{\alpha}$-SREBP-1c pathway that leads to hepatic steatosis. In addition, the anti-lipogenic potential may, at least in part, be associated with activation of Nrf2.
The aim of this study was to investigate the effects of P/S ratio of fatty acid and antioxidant (vitamin E, selenium) supplements on the serum lipid levels and hepatic antioxidant enzyme activity in rats. Female 16-week-old Sprague-Dawley rats were fed 6 different experimental diets for 4 weeks. While the peroxidizability index (PI) levels of fatty acids in the experimental diets were fixed at 81.22, the levels of P/S ratio of fatty acids were formulated at 0.38, 1.00, 4.81 (LP, MP, HP). These diets were supplemented with vitamin E (1,000 mg/kg diet) and selenium (2.5 mg/kg diet) (LP-S, MP-S, HP-S). This study showed that the serum concentrations of total-cholesterol and HDL-C increased with the increasing of the P/S ratio in the diet (p <0.05). Antioxidant supplementation significantly lowered the concentrations of triglyceride (TG) and VLDL-C of serum (p<0.05). Levels of thiobarbituric acid reactive substance (TBARS) in the liver tended to decrease with the increasing of the P/S ratio in the diet (p<0.001), but antioxidant enzyme activity in the liver was not significantly different. In addition, antioxidant supplementation significantly lowered TBARS level in the liver (p<0.05), but had no effect on antioxidant enzyme activity except for glutathione reductase (p<0.05). In conclusion, it is necessary to consider the properties of dietary fatty acids and antioxidants supplementation for the prevention of cardiovascular diseases.
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