The 10trans, 12cis isomer of conjugated linoleic acid promotes energy metabolism in OLETF rats

OBJECTIVE: We investigated the effect of conjugated linoleic acid (CLA) on energy metabolism in Otsuka Long-Evans Tokushima Fatty (OLETF) rats. METHODS: In experiment 1, male OLETF rats were fed either control diet, 10% safflower oil or CLA diet, 9% safflower oil plus 1% CLA for 4 wk. In experiment 2, male OLETF rats were fed either 9c,11t-CLA diet, 9% safflower oil plus 1% 9c,11t-CLA-rich oil or 10t,12c-CLA diet, 9% safflower oil plus 1% 10t,12c-CLA-rich oil for 10 d. RESULTS: In experiment 1, after 4 wk of feeding, serum and hepatic triacylglycerol concentrations in the CLA group were decreased significantly as compared with the control group. The CLA diet increased oxygen consumption and energy expenditure as compared with the control diet in OLETF rats. In experiment 2, a significant reduction of serum and hepatic triacylglycerol concentrations was seen in the 10t,12c-CLA group as opposed to the 9c,11t-CLA group. Oxygen consumption and energy expenditure were significantly higher in the 10t,12c-CLA group than in the 9c,11t-CLA group. CONCLUSIONS: These results demonstrated that the hypolipidemic effect and the enhancement of energy metabolism by CLA can be attributed to the effect of the 10t,12c-CLA isomer.     

Trans10,cis12-18:2 is a more potent inhibitor of de novo fatty acid synthesis and desaturation than cis9,trans11-18:2 in the mammary gland of lactating mice

To investigate the effects of 2 conjugated linoleic acid (CLA) isomers and trans11-18:1 (TVA) on de novo lipogenesis and desaturation in liver and mammary gland, lactating mice were fed diets containing 3% canola oil (control) or 2% canola oil plus 1% stearic acid (SA), TVA, cis9,trans11 CLA (c9t11), or trans10,cis12 CLA (t10c12). In mammary tissue, TVA and CLA isomers reduced mRNA for acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS) compared with control, but only c9t11 and t10c12 reduced mammary ACC activity. Of the 2 CLA isomers, t10c12 caused a greater reduction in mammary ACC activity. Hepatic ACC or FAS activity and mRNA abundance were not affected by dietary treatments. Feeding TVA, c9t11, or t10c12 reduced mammary stearoyl-CoA desaturase 1 (SCD) mRNA and activity. Reduction was greater due to feeding t10c12 compared with c9t11. Hepatic SCD mRNA was not affected by dietary treatments, but both CLA isomers depressed hepatic SCD activity. Results indicated that t10c12 is a more potent inhibitor of mammary lipogenesis and desaturation than is c9t11. A net gain of 77 and 1690 micro g of c9t11 in liver and mammary tissue, respectively, was found in the TVA-fed group over the control and SA-fed group. However, reduced mammary SCD mRNA or activity due to feeding TVA may indicate a limited capacity for desaturation of dietary TVA to c9t11 in vivo.     

The cholesterolaemic effects of dietary fats in cholesteryl ester transfer protein transgenic mice.

In order to investigate the role of cholesteryl ester transfer protein (CETP) in the cholesterolaemic response to dietary fats, we analysed plasma lipid profiles of CETP-transgenic and control C57BL/6 mice fed standard chow (AIN-93G; AIN), a low-fat diet, and diets high in butter (saturated fatty acids; SFA), high-oleic acid safflower oil (monounsaturated fatty acids; MUFA), and safflower oil (polyunsaturated fatty acids; PUFA) for 5 weeks. Each group contained four or five mice. There were significant diet and dietxgenotype effects on plasma total cholesterol (TC; and respectively), liver TC ( and respectively), and esterified cholesterol (EC; and respectively); diet effects on plasma triacylglycerol liver free cholesterol and body weight a genotype effect on body-weight gain and a dietxgenotype effect on energy intake In transgenic mice the SFA diet caused significantly higher plasma TC than the PUFA diet In control mice MUFA and PUFA diets, but not the SFA diet, caused significantly higher plasma TC than the low-fat and AIN diets Transgenic mice fed PUFA had lower plasma TC while transgenic mice fed MUFA had lower LDL+VLDL-cholesterol than controls in the same dietary groups. Transgenic mice fed MUFA and PUFA diets also had significantly higher liver TC and respectively) and EC and respectively) than controls fed the same diets. In the present study we showed that: (1) CETP transgenic mice had a cholesterolaemic response to dietary fats similar to that in human subjects; (2) CETP transgenic mice fed PUFA showed significantly lower plasma TC, while those fed MUFA had lower LDL+VLDL-cholesterol than controls; (3) hepatic accumulation of cholesterol, possibly resulting from the combination of the enhanced cholesteryl ester transfer to apolipoprotein B-containing lipoproteins and increased hepatic uptake of cholesterol, may contribute to the cholesterol-lowering effect of MUFA and PUFA in CETP-transgenic mice; (4) CETP may play a role in appetite and/or energy regulation.     

不同膳食油脂对高脂血症大鼠脂质代谢影响的比较研究

目的比较4种脂肪酸组成迥异的膳食油脂对高脂血症大鼠脂质代谢的影响,并初步探讨其作用机制。方法将OLETF大鼠28只分为4组,喂以AIN76基本配方饲料,基础油脂含量为8%,各组分别添加2%棕榈油、琉璃苣油、紫苏油和鱼油。4 w后,测定大鼠空腹血清甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)、游离脂肪酸(NEFA)、葡萄糖浓度,肝脏TG、TC、磷脂(PL)浓度以及肝脏脂质代谢相关酶脂肪酸合成酶(FAS)、苹果酸酶(ME)、葡萄糖6磷酸脱氢酶(G6PDH)和肉碱棕榈酰转移酶(CPT-1,CPT-2)的mRNA表达。结果与棕榈油组比,琉璃苣油组血清中NEFA、TG含量显著降低(P<0.05),TC、HDL-C含量明显升高(P<0.05)。紫苏油组血清中NEFA、TG含量显著降低(P<0.05)。鱼油组与其它组相比,各项指标含量均显著降低(P<0.05)。琉璃苣油和紫苏油组可明显降低肝脏TG和TC浓度(P<0.05),鱼油组显著降低肝脏TG浓度(P<0.05),对TC浓度无明显影响。此外,琉璃苣油、紫苏油和鱼油组可显著抑制肝脏脂肪合成相关酶的mRNA表达(P<0.05),同时显著增加脂肪酸分解酶mRNA表达(P<0.05)。结论相比于棕榈油组,摄食琉璃苣油、紫苏油和鱼油可通过抑制肝脏脂肪酸合成和促进脂肪酸分解,降低高脂血症大鼠血清和肝脏脂肪水平。     

Effects of fat emulsions with different fatty acid composition on plasma and hepatic lipids in rats receiving total parenteral nutrition

Effects of different fatty acids on the development of hepatic steatosis were studied in rats receiving total parenteral nutrition (TPN). 65 rats, with internal jugular catheters, were divided into one control group (n = 8), and four experimental groups (n = 13-15 each). The control group was fed a chow diet and all experimental groups received TPN. TPN provided 300 kcal/kg/day with 40% of the non-protein energy provided as fat. All TPN solutions were isonitrogenous and identical in nutrient composition except for the fatty acid composition of the fat emulsion. Four kinds of fat emulsions rich in: 1) medium chain fatty acids (C8:0,C10:0), 2) oleic acid (C18:1 n-9), 3) linoleic acid (C18:2 n-6), 4) eicosapentaenoic acid (C20:5 n-3)/docosahexaenoic acid (C22:6 n-3), were used. These fat emulsions were prepared with: 1) a mixture of medium chain triglycerides (MCT) and soybean oil (9:1), 2) olive oil, 3) safflower oil, 4) fish oil, respectively. The results of the study demonstrated a higher hepatic lipid content in the olive oil and safflower oil groups than in the control group, whereas no significant difference was seen between the MCT and control groups. Also, no difference was observed between the fish oil and control groups. With regard to the plasma lipids, the MCT group and olive oil group produced hyperlipidaemia. The plasma of the safflower oil and fish oil groups, however, had a low lipid concentration comparable to the control group. These results suggest that TPN with a fat emulsion prepared with fish oil does not cause hyperlipidaemia nor induce hepatic steatosis in normal rats.     

石榴皮多酚提取物降血脂效果的实验研究

目的提取和富集石榴皮中的多酚类物质，并探讨其降血脂效果。方法采用乙酸乙酯萃取石榴皮粗提取物中的多酚类物质并富集，以高脂饲料喂养雄性SD大鼠建立高脂血症模型，观察饲料补充提取物喂养28d对大鼠血脂和肝脂水平的影响。结果石榴皮粗提取物经进一步分离提取后，多酚类物质得到了富集。高脂组大鼠经多酚提取物饲养后，其血清TC、TG、LDL—C、FFA和肝TC、TG、FFA比高脂对照组分别减少42．4％、58．5％、48．9％、20．6％和32．6％、11．9％、25．5％。部分作用有强于石榴皮粗提取物的趋势，而且还具有提高血清高密度脂蛋白胆固醇(HDL—C)水平的作用。结论石榴皮多酚提取物具有降低血脂和肝脂的作用，有效成分有待进一步分析。     

Hepatic cholesterol and fatty acid synthesis in pregnant and fetal rats: effect of maternal dietary fat and cholestyramine.

Previous studies from this laboratory have demonstrated that 20% rather than 5% (wt/wt) safflower oil or addition of 5% (wt/wt) cholestyramine to the diet of pregnant rats leads to an increase in the activity of 3-hydroxy-3-methylglutaryl CoA reductase, the rate-limiting enzyme of cholesterol synthesis, in the fetal liver. Total cholesterol, however, was not altered in fetal plasma or liver. The effect of these diets on cholesterol and fatty acid synthesis in vivo was therefore studied in fetal and maternal liver. In fetuses of rats fed a reference nonpurified diet, rates of hepatic cholesterol and fatty acid synthesis decreased from gestation d 20 to 21. In contrast, total and active 3-hydroxy-3-methyl-glutaryl CoA reductase activity increased. Adding cholestyramine to the diet or modifying the quantity of safflower oil fed had no effect on fetal hepatic lipogenesis. Maternal hepatic cholesterol synthesis was greater in rats fed cholestyramine, whereas fatty acid synthesis was lower in the dams fed the diet containing 20% compared with 5% safflower oil. The results suggest near-term fetal liver 3-hydroxy-3-methylglutaryl CoA reductase activities do not reflect fetal cholesterol synthesis in vivo.     

Hepatic fatty acid metabolism in rats fed diets with different contents of C18:0, C18:1 cis and C18:1 trans isomers

In the present study the effects of some C18 fatty acids on hepatic fatty acid metabolism have been compared. Male rats were fed cholesterol-free diets containing either C18:0, C18:1 cis or C18:1 trans isomers as the variables. In accordance with previous work, oleic acid in the diet caused an increase in cholesterol concentration in the liver and in the lipoprotein fraction of density (d; kg/l) < 1.006. Oleic acid also reduced the triacylglycerol:cholesterol value in this fraction. Surprisingly, the C18:1 trans isomers diet induced a decrease in the amount of cholesterol in total plasma as well as in the 1.019 < d < 1.063 lipoprotein fraction. Both oleic acid and C18:1 trans isomers increased the concentration of triacylglycerols in the liver. The two C18:1 fatty acids differently influenced the hepatic activities of carnitine palmitoyltransferase-I and 3-hydroxy-acyl-CoA dehydrogenase; both enzymes were inhibited by C18:1 trans isomers, while no change was induced by oleic acid. The activity of the citrate carrier was lower in the oleic acid- and C18:1 trans isomers-fed rats, when compared with the rats fed stearic acid. No diet effects were seen for the activities of acetyl-CoA carboxylase, fatty acid synthase, diacylglycerol acyltransferase, citrate synthase and phosphofructokinase. The results are interpreted in that oleic acid raised liver triacylglycerol by reducing the secretion of it with the d < 1.006 lipoprotein fraction whereas the C18:1 trans isomers enhanced liver triacylglycerol by lowering the hepatic oxidation of fatty acids.     

Less body fat accumulation in rats fed a safflower oil diet than in rats fed a beef tallow diet

The effects on body fat accumulation of long-term feeding of high fat diets of differing fatty acid composition were studied in rats. The rats were meal-fed isoenergetic diets based on safflower oil or beef tallow for 4 mo. Each diet was freshly prepared every day throughout the experimental period. Oxygen consumption and carbon dioxide production for 6 h after meals were measured between the 50th and 54th d of the experimental period. Oxygen consumption for 3 h after meals was significantly greater in the safflower oil diet group than in the beef tallow diet group, indicating greater diet-induced thermogenesis in the former group. From the assessment of respiratory quotient, the fat oxidation rate was also higher in the former. After the experimental period (4 mo), body fat accumulation was significantly less in the rats fed safflower oil. This difference was, at least in part, ascribed to increased diet-induced thermogenesis and fat oxidation. Serum triacylglycerol level was markedly lower in the rats fed safflower oil than in those fed beef tallow. The lipoprotein lipase activities in heart and soleus muscle after meals appeared to be higher in the former than in the latter. These results suggest that the consumption of the safflower oil diet increased lipoprotein lipase activity in heart and skeletal muscle, resulting in the elevation of fat oxidation rate and the depression of serum triacylglycerol level.     

Antihyperglycemic effect of stem bark powder from paper mulberry (Broussonetia kazinoki Sieb.) in type 2 diabetic Otsuka Long-Evans Tokushima fatty rats

The effect of stem bark powder from paper mulberry (PMSB) on serum glucose, insulin, fructosamine, and lipid concentrations, as well as enzyme activities that serve as liver injury markers, was investigated in genetically diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats. Both nondiabetic Long-Evans Tokushima Otsuka (LETO) rats and diabetic OLETF rats (30 weeks old) were fed a semisynthetic diet with or without 50 g/kg PMSB for 8 weeks and then compared. The OLETF control rats showed a high amount of daily water intake in comparison to those in the LETO group. The concentrations of glucose, fructosamine, total lipid, triglyceride, total cholesterol, and high-density lipoprotein-cholesterol and the activities of aspartate aminotransferase and alanine aminotransferase (ALT) in serum were higher in the OLETF control rats than those in the LETO control rats. However, PMSB ingestion decreased the serum levels of glucose, fructosamine, triglyceride, and total cholesterol and the activity of ALT in the OLETF rats, but not in the LETO rats. The concentration of serum insulin was also significantly increased by PMSB consumption in the OLETF rats compared to the OLETF control rats. These results suggest that PMSB might have an antihyperglycemic effect in the OLETF rat and that the increased blood insulin level would be an important regulatory factor for improving hyperglycemia in the current animal model.     

Suppression of rat liver fatty acid synthesis by eicosa-5,8,11,14-tetraynoic acid without a reduction in lipogenic enzymes

In meal-fed rats supplementation of safflower oil (5 g per 100 g diet) to a fat-free basal diet resulted in the characteristic suppression of liver fatty acid synthetase and acetyl-CoA carboxylase activities, which was accompanied by a 60% decrease in the rate of hepatic fatty acid synthesis. The decline in activity of these lipogenic enzymes was completely prevented by adding 0.05% eicosa-5,8,11,14-tetraynoic acid (TYA) to the safflower oil diet. Fatty acid analysis of the livers indicated that TYA significantly impaired the conversion of linoleate to arachidonate. Apparently the selective suppression of lipogenic enzymes by dietary linoleate is not caused by linoleate per se but requires its conversion to longer-chain fatty acids and/or protaglandins. In spite of high activities of fatty acid synthetase and acetyl-CoA carboxylase, liver fatty acid synthesis continued to be inhibited by the safflower oil + TYA dietary regimen. This continued inhibition of lipogenesis was due to the TYA, because addition of TYA to the fat-free diet precipitated a significant decline in liver fatty acid synthesis without a drop in lipogenic enzymes. Inhibition of fatty acid synthesis by TYA could not be attributed to a decrease in liver glucose utilization based on hepatic glycogen concentration, nor was it due to a reduction in the fraction of catalytically active polymeric acetyl-CoA carboxylase based on sensitivity of the enzyme activity to avidin.     

Accumulation and apparent oxidation of cis,trans-18 : 2 isomers relative to linoleic acid in rats

Dietary cis,trans-18 : 2 isomers impair desaturation and elongation of linoleic acid (Delta9cis,12cis-18 : 2), but little is known of their proportional partitioning between accumulation and oxidation. The present study was therefore designed to assess the accumulation and apparent oxidation of cis,trans-18 : 2 isomers compared with that of trans-18 : 1 isomers and Delta9cis,12cis-18 : 2 in rats. Accumulation is defined as whole-body increase in a fatty acid during a given period (i.e. final body content-initial body content). The apparent oxidation (disappearance) is defined as whole-body utilization of a fatty acid relative to its intake for a given period (intake-excretion-accumulation-longer-chain products)/intakex100). The animals were fed on a diet containing 15 % (w/w) partially hydrogenated rapeseed oil with 1.72 % energy as cis,trans-18 : 2 isomers and varying amounts of Delta9cis,12cis-18 : 2. The apparent oxidation of total cis,trans-18 : 2 isomers (72-76 % dietary intake) was greater than that of Delta9cis,12cis-18 : 2 (38-51 % dietary intake) but it was similar to that of total trans-18 : 1 isomers (78-82 % dietary intake). Among the four isomers, the apparent oxidation of Delta9trans,12trans-18 : 2 was greater than that of the other isomers including Delta9trans,12cis-18 : 2, Delta9cis,12trans-18 : 2 and Delta9cis,13trans-18 : 2. Accumulation of Delta5cis,8cis,11cis,15trans-20 : 4 and Delta5cis,8cis,11cis,14trans-20 : 4 derived from chain-elongation and desaturation of Delta9cis,13trans-18 : 2 and Delta9cis,12trans-18 : 2 was decreased when the dietary Delta9cis,12cis-18 : 2 supply was increased.     

Inhibition of liver lipogenesis by dietary polyunsaturated fat in severely diabetic rats

Diabetic and nondiabetic rats were used to ascertain if dietary polyunsaturated fats inhibited hepatic acetyl-CoA carboxylase and fatty acid synthetase in insulin-insufficient rats as had been previously shown for normal rats. Male rats were rendered diabetic (400-600) mg glucose/100 mL blood) with streptozotocin and were fed a high fructose fat-free diet. Safflower oil or palmitate (or tallow) was added to the basal fructose diet at a level to supply 12,24 or 36% additional digestible energy. Compared with normal rats, diabetic rats had significantly lower hepatic fatty acid biosynthesis, but the proportion of acetyl-CoA carboxylase expressing catalytic activity as determined by the avidin-inactivation technique was unaffected by diabetes. Diabetes did not lower the maximal maximal activities of carboxylase and fatty acid synthetase. Moreover, the activities of these enzymes greatly exceeded the rate of fatty acid synthesis. At all levels of fat supplementation, the high linoleate safflower oil consistently resulted in a 50% lower rate of fatty acid biosynthesis than did comparable levels of tallow or palmitate. Safflower oil was also a more effective suppressor of the activities of acetyl-CoA carboxylase and fatty acid synthetase than the saturated fats. Our data suggest that the greater inhibition of hepatic fatty acid biosynthesis by polyenoic fatty acids is an insulin-independent mechanism.     

Dietary oxidized fat prevents ethanol-induced triacylglycerol accumulation and increases expression of PPARalpha target genes in rat liver

Alcoholic fatty liver results from an impaired fatty acid catabolism due to blockade of PPARalpha and increased lipogenesis due to activation of sterol regulatory element-binding protein (SREBP)-1c. Because both oxidized fats (OF) and conjugated linoleic acids (CLA) have been demonstrated in rats to activate hepatic PPARalpha, we tested the hypothesis that these fats are able to prevent ethanol-induced triacylglycerol accumulation in the liver by upregulation of PPARalpha-responsive genes. Forty-eight male rats were assigned to 6 groups and fed isocaloric liquid diets containing either sunflower oil (SFO) as a control fat, OF prepared by heating of SFO, or CLA, in the presence and absence of ethanol, for 4 wk. Administration of ethanol lowered mRNA concentrations of PPARalpha and the PPARalpha-responsive genes medium chain acyl-CoA dehydrogenase, long chain acyl-CoA dehydrogenase, acyl-CoA oxidase, carnitine palmitoyl-CoA transferase I, and cytochrome P450 4A1 and increased triacylglycerol concentrations in the liver (P < 0.05). OF increased hepatic mRNA concentrations of PPARalpha-responsive genes and lowered hepatic triacylglycerol concentrations compared with SFO (P < 0.05) whereas CLA did not. Rats fed OF with ethanol had similar mRNA concentrations of PPARalpha-responsive genes and similar triacylglycerol concentrations in the liver as rats fed SFO or CLA without ethanol. In contrast, hepatic mRNA concentrations of SREBP-1c and fatty acid synthase were not altered by OF or CLA compared with SFO. This study shows that OF prevents an alcohol-induced triacylglycerol accumulation in rats possibly by upregulation of hepatic PPARalpha-responsive genes involved in oxidation of fatty acids, whereas CLA does not exert such an effect.     

Alpha-linolenic acid but not conjugated linolenic acid is hypocholesterolaemic in hamsters

Conjugated linolenic acid (CLN) refers to a group of octadecatrienoic acid isomers that have three double bonds in conjugation. Both pomegranate and tung seed oils are rich in CLN but the major isomer in the former is cis9,trans11,cis13 while in the latter it is cis9,trans11,trans13. The present study examined the effects of CLN, isolated from either pomegranate seed oil or tung seed oil, and alpha-linolenic acid (LN), isolated from flaxseed oil, on serum cholesterol levels in male hamsters (body weight 105 g; age 10 weeks) fed a 0.1% cholesterol and 10% lard diet, for a period of 6 weeks. All hamsters were allowed free access to food and fluid. The blood samples were taken by bleeding from the retro-orbital sinus into a heparinized capillary tube under light ether anaesthesia after overnight fasting at weeks 0, 2, 4 and 6. It was found that supplementation of CLN at levels of 12.2-12.7 g/kg diet exhibited no significant effect on serum cholesterol level while LN at a similar level of supplementation had serum cholesterol reduced by 17-21% compared with the control diet containing no LN and CLN. Supplementation of CLN and LN significantly decreased hepatic cholesterol but no effect was observed on heart and kidney cholesterol levels. It was concluded that LN possessed hypocholesterolaemic activity while CLN had no effect on blood cholesterol, at least in hamsters.     

Potency of polyunsaturated and saturated fats as short-term inhibitors of hepatic lipogenesis in rats

Three dietary studies using male Sprague-Dawley rats conditioned to meal-eat a high glucose, fat-free diet and one in vitro study with isolated rat hepatocytes were designed to examine the hypothesis that polyunsaturated fats (i.e., safflower oil or linoleate) are more potent acute inhibitors of liver fatty acid synthesis than are saturated fats (i.e., beef tallow or palmitate). Fat in the first in vivo study was administered via intubation (1500 mg/rat) whereas in the second and third in vivo studies fat was added to the meal in amounts of 50, 100, 250 or 500 mg/g fat-free diet. When the rats were in a postprandial condition, significant suppression of hepatic lipogenesis required the meal to contain 38% of its energy as fat (i.e., 250 mg/g fat-free diet). At this level of fat, safflower oil was more inhibitory than beef tallow (p less than 0.05). The inhibition constant (Ki) for palmitate inhibition of fatty acid synthesis by isolated hepatocytes was fourfold greater than linoleate's Ki (fatty acid/albumin ratio of 1.4/1). When fat constituted 50% of the ingested energy, beef tallow was equivalent to safflower oil as an inhibitor of lipogenesis. Although a single meal containing 50 mg safflower oil/g fat-free diet did not decrease fatty acid synthesis, it effectively delayed the induction of lipogenesis during the first 30 min of the adaptive decrease in lipogenic enzymes attributed to polyunsaturated fats extends to short-term regulatory mechanisms.     

Eicosapentaenoic acid and 3,10 dithia stearic acid inhibit the desaturation of trans-vaccenic acid into cis-9, trans-11-conjugated linoleic acid through different pathways in Caco-2 and T84 cells

Stearoyl-CoA desaturase (SCD) is a key enzyme that determines the composition and metabolic fate of ingested fatty acids, in particular the conversion of trans-vaccenic acid (TVA) to conjugated linoleic acid (CLA). The present study addressed the hypothesis that intestinal TVA absorption and biotransformation into CLA can be modulated by EPA and 3,10-dithia stearic acid (DSA) via altered SCD mRNA levels and desaturation indices (cis-9, trans-11-CLA:TVA and oleic acid:stearic acid ratios) in Caco-2 and T84 cells, two well-established in vitro models of the human intestinal epithelium. The study determined the effect of acute (3 h with 0.3 mm-EPA or 0.3 mm-DSA) and acute-on-chronic (1 week with 0.03 mm-EPA or -DSA, followed by respectively, 0.3 mm-EPA or -DSA for 3 h) treatments. In both cell lines, acute EPA treatment did not alter SCD desaturation indices, whereas the acute-on-chronic treatment affected these surrogate markers of SCD activity. This was associated with reduced sterol regulatory-element binding protein-1c and SCD mRNA levels. In contrast, acute and acute-on-chronic DSA treatments significantly reduced SCD desaturation indices without affecting SCD mRNA levels in Caco-2 cells. The present study on intestinal cells shows that the conversion rate of TVA to c9, t11-CLA is affected by other fatty acids present in the diet such as EPA, confirming previous observations in hepatic and mammary cell models.     

Dietary phospholipid-dependent reductions in gene expression and activity of liver enzymes in fatty acid synthesis in fasted-refed rats.

The effects of dietary soybean phospholipid, its hydrogenation product and safflower phospholipid on gene expression and the activity of hepatic enzymes in fatty acid biosynthesis were examined in fasted-refed rats. Phospholipid composition of soybean phospholipid and its hydrogenation product were the same, but the hydrogenation product contained negligible amounts of unsaturated fatty acids. Among phospholipid classes, lysophosphatidylcholine and phosphatidylinositol proportions were slightly higher in safflower phospholipid than in soybean phospholipid or its hydrogenation product. Rats were fasted for 2 d and refed a fat-free diet or a diet containing 4% fatty acids either as soybean oil or various phospholipid preparations for 3 d. Compared to the fat-free diet, the soybean oil diet only slightly decreased specific, but not total hepatic fatty acid synthetase and malic enzyme activity, and it was totally ineffective in modulating glucose 6-phosphate dehydrogenase and pyruvate kinase activity under our experimental conditions. The diets containing phospholipids, however, markedly decreased the activity of these enzymes. The extent of reduction was somewhat attenuated with hydrogenated soybean phospholipid as compared with soybean and safflower phospholipids. Dot and Northern blot hybridization using specific cDNA probes showed that, compared to a fat-free diet, diets containing phospholipids profoundly decreased the hepatic mRNA levels of enzymes in fatty acid synthesis. Soybean oil, however, only marginally affected these parameters. Hepatic mRNA levels for enzymes correlated well with enzyme activity. Dietary phospholipids therefore appear to have decreased enzyme activity in fatty acid synthesis primarily by suppressing the mRNA levels of these enzymes. Compared to soybean oil, hydrogenated soybean phospholipid is still effective in decreasing the activity and mRNA level of enzymes in fatty acid synthesis. Therefore, it is difficult to ascribe the potent physiological activity of phospholipid in reducing fatty acid synthesis entirely to polyunsaturated fatty acid moiety.     

Dietary fish oil and Undaria pinnatifida (wakame) synergistically decrease rat serum and liver triacylglycerol

Japanese eating habits are characterized by the consumption of various food materials such as cereals, vegetables, fish, shellfish, marine algae and meat. Therefore, properties of functional substances in food materials may be enhanced or lessened by the combination of various food materials. In the present study, we examined how the combination of wakame and fish containing polyunsaturated fatty acids, which are typical Japanese food materials, affected rat lipid metabolism. Rats were fed one of four diets [control diet (C), AIN-76 diet with 5 g/100 g rapeseed oil; wakame diet (W) containing 19.1 g/100 g Undaria pinnatifida (wakame) dried powder in the C diet; fish oil diet (FO), AIN-76 diet with 4.1 g/100 g fish oil; wakame-fish oil diet (W + FO), the FO diet containing 19.1 g/100 g dried wakame powder] for 4 wk. We measured the concentration of lipids in serum and liver and hepatic activities of enzymes involved in fatty acid metabolism. The W diet, FO diet and W + FO diet significantly reduced the concentration of triacylglycerols in the serum and liver compared with the C diet. This decrease in the concentration of hepatic triacylglycerol was greatest in rats fed the W + FO diet. The activity of glucose-6-phosphate dehydrogenase, which is involved in fatty acid synthesis in the liver, of rats fed the W, FO and W + FO diets was lower than that in rats fed the C diet. However, the activities of malic enzyme and fatty acid synthetase did not differ among the four groups. In contrast, the W diet and W + FO diet increased the serum concentration of beta-hydroxybutyrate. Further, the activity of 3-hydroxyacyl-CoA dehydrogenase, which is involved in fatty acid beta-oxidation in the liver, was greater in rats fed the W diet (42%), the FO diet (154%) and the W + FO diet (381%) than in those fed the C diet. Because the decrease in the concentration of triacylglycerol in the liver was greatest when rats were fed wakame and fish oil at the same time (W + FO diet), we conclude that there was a synergistic process affecting fatty acid beta-oxidation in the liver. These results suggest that the simultaneous consumption of fish (fish oil) and wakame decreases the concentration of triacylglycerol in the serum and liver.