Effects Of Fish Oil Feeding Research Articles

Improvement in in vitro fertilization rate, decrease in reactive oxygen species and spermatozoa death incidence in rams by dietary fish oil.

Our aim was to evaluate the effects of fish oil feeding on sperm classical parameters, level of reactive oxygen spices (ROS), spermatozoa death incidence and in vitro fertilization (IVF) rate in rams. We randomly assigned nine rams, into two experimental groups (isoenergetic and isonitrogenous rations with constant level of vitamin E supplement): control (CTR; n = 5) and fish oil (FO; n = 4, 35 g/day/ram). Diets were fed for 70 days during the physiological breeding season. After a 21-day dietary adaptation period, semen was collected weekly from each ram by an artificial vagina. Sperm classical parameters were determined by the computer-assisted sperm analyzer system (CASA), and it was prepared for IVF process by swim-up technique. These evaluations were performed during the first and last weeks of sampling. Intracellular ROS level and spermatozoa death incidence were detected by flow cytometry on a weekly basis after adaptation. Data were analysed with SPSS 15. The volume, concentration (3.6 and 2.7 × 10(9) /ml) and sperm progressive motility (60 and 48%) were significantly improved in the FO group compared with the CTR (p < 0.05). A comparison of two-cell stage embryos following IVF in the two groups showed a significantly higher fertilization rate in the FO group (56%) compared with the CTR (49%). Superoxide anion (O2 (-) ) rate was significantly lower (p < 0.05) at the third week of sampling in the FO. Although the H2 O2 rate was numerically lower in the FO group compared with the CTR, this difference was not significant. In addition, apoptosis showed a significant difference in the third week of sampling (15 and 30% for FO and CTR, respectively; p < 0.05). Overall, adding fish oil to the ram diet not only improved sperm quality and IVF results, it also could reduce oxygen-free radicals and the incidence of spermatozoa death.

Fish Oil-Fed Mice Have Impaired Resistance to Influenza Infection ,

Dietary fish oils, rich in (n-3) PUFA, including eicosapentaenoic acid and docosahexaenoic acid, have been shown to have antiinflammatory properties. Although the antiinflammatory properties of fish oil may be beneficial during a chronic inflammatory illness, the same antiinflammatory properties can suppress the inflammatory responses necessary to combat acute viral infection. Given that (n-3) fatty acid-rich fish oil supplementation is on the rise and with the increasing threat of an influenza pandemic, we tested the effect of fish oil feeding for 2 wk on the immune response to influenza virus infection. Male C57BL/6 mice fed either a menhaden fish oil/corn oil diet (4 g fish oil:1 g corn oil, wt:wt at 5 g/100 g diet) or a control corn oil diet were infected with influenza A/PuertoRico/8/34 and analyzed for lung pathology and immune function. Although fish oil-fed mice had lower lung inflammation compared with controls, fish oil feeding also resulted in a 40% higher mortality rate, a 70% higher lung viral load at d 7 post infection, and a prolonged recovery period following infection. Although splenic natural killer (NK) cell activity was suppressed in fish oil-fed mice, lung NK activity was not affected. Additionally, lungs of infected fish oil-fed mice had significantly fewer CD8+ T cells and decreased mRNA expression of macrophage inflammatory protein-1-α, tumor necrosis factor-α, and interleukin-6. These results suggest that the antiinflammatory properties of fish oil feeding can alter the immune response to influenza infection, resulting in increased morbidity and mortality.

Regulation of intestinal NPC1L1 expression by dietary fish oil and docosahexaenoic acid

To address the effect of the n-3 fatty acid, docosahexaenoic acid (22:6), on proteins that play a role in cholesterol absorption, CaCo-2 cells were incubated with taurocholate micelles alone or micelles containing 22:6 or oleic acid (18:1). Compared with controls or 18:1, 22:6 did not interfere with the cellular uptake of micellar cholesterol. Apical cholesterol efflux was enhanced in cells incubated with 22:6. Cholesterol trafficking from the plasma membrane to the endoplasmic reticulum was decreased by 22:6. 22:6 decreased Niemann-Pick C1-Like 1 (NPC1L1) protein and mRNA levels without altering gene or protein expression of ACAT2, annexin-2, caveolin-1, or ABCG8. Peroxisome proliferator-activated receptor delta (PPARdelta) activation decreased NPC1L1 mRNA levels and cholesterol trafficking to the endoplasmic reticulum, suggesting that 22:6 may act through PPARdelta. Compared with hamsters fed a control diet or olive oil (enriched 18:1), NPC1L1 mRNA levels were decreased in duodenum and jejunum of hamsters ingesting fish oil (enriched 22:6). In an intestinal cell, independent of changes in ABCG8 expression, 22:6 increases the apical efflux of cholesterol. 22:6 interferes with cholesterol trafficking to the endoplasmic reticulum by the suppression of NPC1L1, perhaps through the activation of PPARdelta. Moreover, a diet enriched in n-3 fatty acids decreases the gene expression of NPC1L1 in duodenum and jejunum of hamster.

Fish Oil Regulates Adiponectin Secretion by a Peroxisome Proliferator–Activated Receptor-γ–Dependent Mechanism in Mice

Adiponectin has insulin-sensitizing, antiatherogenic, and anti-inflammatory properties, but little is known about factors that regulate its secretion. To examine the effect of fish oil on adiponectin secretion, mice were fed either a control diet or isocaloric diets containing 27% safflower oil or 27, 13.5, and 8% menhaden fish oil. Within 15 days, fish oil feeding raised plasma adiponectin concentrations two- to threefold in a dose-dependent manner, and the concentrations remained approximately twofold higher for 7 days when the fish oil diet was replaced by the safflower oil diet. Within 24 h, fish oil markedly induced transcription of the adiponectin gene in epididymal adipose tissue but not in subcutaneous fat. The increase of plasma adiponectin by fish oil was completely blocked by administration of the peroxisome proliferator-activated receptor (PPAR)gamma inhibitor bisphenol-A-diglycidyl ether. In contrast, there was no effect of fish oil feeding on adiponectin secretion in PPARalpha-null mice. These data suggest that fish oil is a naturally occurring potent regulator of adiponectin secretion in vivo and that it does so through a PPARgamma-dependent and PPARalpha-independent manner in epididymal fat.

Comparative Effect of Fish Oil Feeding and Other Dietary Fatty Acids on Plasma Lipoproteins, Biliary Lipids, and Hepatic Expression of Proteins Involved in Reverse Cholesterol Transport in the Rat

Background: While elevated plasma high-density lipoprotein (HDL) levels has been associated to a reduction in cardiovascular risk, dietary fish oils rich in omega–3 polyunsaturated fatty acids (PUFAs) may protect against this disease. The protective effect of HDL is associated to its participation in the reverse cholesterol transport pathway. On the other hand, omega–3 PUFAs decrease plasma HDL levels compared to other fatty acids, which may suggest an effect on reverse cholesterol transport. Aim: In this work, the effect of dietary fish oil on the fatty acid composition of hepatic membranes, plasma lipoprotein cholesterol profile, biliary lipids, and the expression of proteins involved in reverse cholesterol transport, was compared to other dietary oils having a different degree of fatty acid unsaturation. Methods: Male rats were fed a semi synthetic diet containing fish oil (omega–3), sunflower oil (omega–6), olive oil (omega–9) or coconut oil (saturated). Hepatic membrane fatty acid composition, plasma cholesterol levels, lipoprotein cholesterol profile, biliary lipids, hepatic mRNA levels for lecithin cholesterol acyltransferase, hepatic lipase, apo E, and apo A-I, and hepatic protein levels of the scavenger receptor class B type I, caveolin-1, and the ATP binding cassette transporter A1 were analyzed. Plasma apo A-I and apo E protein levels were also evaluated. Results: Compared to the other diets, omega–3 PUFAs significantly changed omega–3/omega–6 fatty acid ratio of hepatic membranes, caused a reduction of plasma total and HDL cholesterol, and selectively increased biliary cholesterol secretion. No modification in the expression levels of lecithin cholesterol acyltransferase, hepatic lipase, apo A-I and apo E mRNA was observed. Hepatic scavenger receptor class B type I, caveolin-1, and the ATP binding cassette transporter A1 protein levels were also not affected. Plasma apo A-I, but not apo E, was reduced. Conclusions: These results show that dietary omega–3 PUFAs reduce plasma HDL cholesterol and increase biliary cholesterol without concomitant modifications in the expression of key genes and proteins involved in reverse cholesterol transport. These findings suggest that functional changes in the activity of these proteins as consequence of the incorporation of omega-3 PUFAs into hepatic membranes and plasma lipoproteins may underlie the effect of fish oil feeding on plasma and hepatic cholesterol metabolism in the rat.

Effects of fish oil feeding and fasting on LXRα/RXRα binding to LXRE in the SREBP-1c promoter in mouse liver

High-fish oil feeding and fasting down-regulate sterol regulatory element-binding protein-1c (SREBP-1c) mRNA level and suppress lipogenesis in mouse liver. Previous promoter analysis revealed that liver X receptor α (LXRα)/retinoid X receptor α (RXRα) complex was required for SREBP-1c gene expression in cell culture. In in vitro studies, polyunsaturated fatty acids (PUFAs, n-6, n-3) inhibited binding of LXRα/RXRα heterodimer to LXR responsive elements (LXREs) in the SREBP-1c promoter. To examine whether fish oil feeding and fasting would also inhibit its binding to LXREs in mouse liver, active liver nuclear extracts were prepared by percoll gradient centrifugation, and gel mobility shift assay was conducted. Although 1- to 5-day fish oil feeding and 2-day fasting decreased SREBP-1c mRNA by 45–68% and 65%, respectively, fish oil feeding decreased binding of LXR/RXR heterodimer to LXREs by 0–26%, while 2-day fasting decreased their binding by 40–56%. Luciferase assay using mutation of LXREs in mouse primary hepatocytes revealed that the LXR ligand, T0901317, induced increased transcription of SREBP-1c mRNA was mediated by LXREs, but it is unknown whether fish oil/eicosapentaenoic acid (EPA)-induced down-regulation of SREBP-1c mRNA was mediated by LXREs. These data indicate that high-fish oil feeding might decrease SREBP-1c mRNA partly by decreased transcription of SREBP-1c, but if so, the binding inhibition of LXRα to LXREs might not be a major cause, while fasting decreased SREBP-1c mRNA, mainly by its binding inhibition of LXRα to LXREs in the SREBP-1c promoter.

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.

Short-Term Feeding of Fish Oil Down-Regulates the Expression of Pyruvate Dehydrogenase E1 Alpha Subunit mRNA in Mouse Brain

Previous studies have suggested that docosahexaenoic acid (DHA), contained in fish oil, prevents brain disease. In the current study, the effect of fish oil feeding on gene expression in the brain was investigated by suppression subtractive hybridization. We found that pyruvate dehydrogenase E1 alpha (PDHE1alpha) mRNA expression is down-regulated by fish oil feeding. We examined whether the expression of PDHE1alpha mRNA is altered by DHA treatment in differentiated PC12 cells. PDHE1alpha mRNA was reduced by supplementation of DHA with a significant decrease in cellular ATP level. These results indicate that fish oil feeding might modulate energy metabolism in the brain.

Fish Oil Feeding Decreases Mature Sterol Regulatory Element-binding Protein 1 (SREBP-1) by Down-regulation of SREBP-1c mRNA in Mouse Liver: A POSSIBLE MECHANISM FOR DOWN-REGULATION OF LIPOGENIC ENZYME mRNAs

Dietary fish oil induces hepatic peroxisomal and microsomal fatty acid oxidation by peroxisome proliferator-activator receptor alpha activation, whereas it down-regulates lipogenic gene expression by unknown mechanism(s). Because sterol regulatory element-binding proteins (SREBPs) up-regulated lipogenic genes, investigation was made on the effects of fish oil feeding on SREBPs and sterol regulatory element (SRE)-dependent gene expression in C57BL/6J mice. Three forms of SREBPs, SREBP-1a, -1c, and -2, are expressed in liver, and their truncated mature forms activate transcription of sterol-regulated genes. C57BL/6J mice were divided into three groups; the first group was given a high carbohydrate diet, and the other two groups were given a high fat diet (60% of total energy), with the fat in the form of safflower oil or fish oil, for 5 months. Compared with safflower oil feeding, fish oil feeding decreased triglyceride and cholesterol concentrations in liver. There were no differences in amount of SREBP-1 and -2 in both precursor and mature forms between carbohydrate- and safflower oil-fed mice. However, compared with safflower oil feeding, fish oil feeding reduced the amounts of precursor SREBP-1 in membrane fraction by 90% and of mature SREBP-1 in liver nuclei by 57%. Fish oil feeding also reduced precursor SREBP-2 by 65% but did not alter the amount of mature SREBP-2. Compared with safflower oil feeding, fish oil feeding decreased liver SREBP-1c mRNA level by 86% but did not alter SERBP-1a mRNA. Consistent with decrease of mature SREBP-1, compared with safflower oil feeding, fish oil feeding down-regulated the expression of liver SRE-dependent genes, such as low density lipoprotein receptor, 3-hydroxy-3-methylglutaryl-CoA reductase, 3-hydroxy-3-methylglutaryl-CoA synthase, fatty acid synthase, acetyl-CoA carboxylase, and stearoyl-CoA desaturase-1. These data suggested that in liver, fish oil feeding down-regulates the mature form of SREBP-1 by decreasing SREBP-1c mRNA expression, with corresponding decreases of mRNAs of cholesterologenic and lipogenic enzymes.

Up-Regulation of Liver Uncoupling Protein-2 mRNA by either Fish Oil Feeding or Fibrate Administration in Mice

Fish oil feeding showed less obesity in rodents, relative to other dietary oils. N-3 fatty acids rich in fish oil and fibrate compounds are peroxisome proliferator-activated receptor α (PPARα) ligands that stimulate β-oxidation of fatty acids in liver and are used for treatment of hypertriglycemic patients. Since UCP-2, a member of an uncoupling protein family, has been shown to express in hepatocytes, the effects of these agents on the expression of UCP2 mRNA were investigated. C57BL/6J mice were divided into three groups; the first group was given a high-carbohydrate diet, and the other two groups were given a high-fat diet (60% of total energy) as safflower oil or fish oil for 5 months. Safflower oil diet fed mice developed obesity, but those fed fish oil diet did not. Therefore, the effects of fish oil feeding on the expression of UCP1, UCP2 and UCP3 in liver, skeletal muscle (gastrocnemius), white adipose tissue (WAT) and brown adipose tissue (BAT) were assessed by Northern blotting. Compared with safflower oil feeding, fish oil feeding up-regulated liver UCP2, BAT UCP2 and skeletal muscle UCP3 mRNA, while down-regulated WAT UCP2 and BAT UCP3 mRNA. Among these alterations, 5-fold up-regulation of liver UCP2 mRNA, relative to carbohydrate feeding, was noteworthy. Fenofibrate administration (about 500 mg/kg BW/d) for 2 wks also induced liver UCP2 expression by 9-fold. These data indicated that fish oil feeding and fibrate administration each up-regulated UCP2 mRNA expression in liver possibly via PPARα and hence each has the potential of increasing energy expenditure for prevention of obesity.

Effects of Fish Oil Feeding Alone in Combination with Clofibric Acid on Serum Levels of Triacylglycerol and Cholesterol in Rats

Rats were fed diets prepared with soybean oil (SO), perilla oil (PO), or fish oil (FO) for 4 weeks, and some of the rats received daily s.c. injections (100mg/kg) of p-chlorophenoxyisobutyric acid (clofibric acid) for 1 week before being killed. The levels of serum triacylglycerol and cholesterol were conspicuously lower in FO-fed rats than in SO-fed rats. The administration of clofibric acid further decreased serum levels of triacylglycerol and cholesterol in SO-fed rats, but not in FO-fed rats. The decreased level of these serum lipids with FO-feeding alone were comparable to those observed in SO-fed rats which had received clofibric acid. The activity of peroxisomal β-oxidation in the liver of FO-fed rats was significantly higher (2.48 times) than that of SO-fed rats. The treatment of FO-fed rats with clofibric acid caused an additional increase in activity, as compared to the SO-fed control. The activity of peroxisomal β-oxidation in SO-fed rats treated with clofibric acid was 3.74 times that of the FO-fed control. In contrast to peroxisomal β-oxidation, the activities of catalase, glutathione (GSH) peroxidase towards hydrogen peroxide and GSH reductase were not increased by clofibric acid, regardless of the type of oil ingested. Moreover, the activities of GSH S-transferases towards 1-chloro-2, 4-dinitrobenzene (CDNB) and 1, 2-dichloro-4-nitrobenzene (DCNB) were both depressed to the same level by the administration of clofibric acid, regardless of the type of dietary oil, although FO-feeding significantly increased the activity of GSH S-transferase towards CDNB. PO comprises essentially the same effects on the parameters tested, to a lesser extent, compared with FO. Consequently, FO-feeding can reduce the dose of clofibric acid required to lower serum lipids, which concomitantly may prevent hepatocytes from oxidative stress that might be caused by an imbalance of hydrogen peroxide metabolism due to the increased activity of peroxisomal β-oxidation and to the decrease in the activities of detoxification by GSH S-transferase.

Fish oil may impede tumour angiogenesis and invasiveness by down-regulating protein kinase C and modulating eicosanoid production

Inhibition of angiogenesis shows considerable promise as a strategy for treating solid malignancies. Induction of collagenase by protein kinase C plays an important role in the angiogenic process as well as in metastasis. Lipoxygenase products are required for endothelial cell mitosis, and also promote collagenase production. By down-regulating hormonal activation of protein kinase C and modulating eicosanoid metabolism, ingestion of omega-3-rich fish oils may impede angiogenesis and reduce tumor invasiveness -thus rationalizing the growth-retardant and anti-metastasic effects of fish oil feeding almost invariably seen in animal tumour models. Certain other anti-inflammatory agents - including cromolyn (an inhibitor of protein kinase C activation) and gamma-linolenic acid (which indirectly inhibits lipoxygenase) may have analogous tumour-retardant activity. Clinical application of supplemental fish oil in cancer therapy is long overdue.

Fish Oil, Alcohol, and Liver Pathology: Role of Cytochrome P450 2E1

Rats were fed ethanol in combination with fish oil or a corn diet in order to evaluate the effect of fish oil feeding on liver injury, microsomal ethanol oxidation, and NADPH-dependent lipid peroxidation. The rats were maintained on the dietary regimen for 72 days, and for comparison, pair-fed controls were studied. The liver pathology score progressively worsened in rats fed alcohol, both in combination with fish oil and corn oil, but the severity of inflammation and focal fibrosis was greater in the ethanol fish oil fed rats as compared with the ethanol corn oil group, whereas the fatty change was greater in the ethanol corn oil fed rats. The alcohol treatment caused a 2-fold increase of the liver microsomal P450 content, and about a similar increase in the rate of microsomal NADPH oxidation. The amount of ethanol-inducible CYP2E1 was about 10-fold higher in alcohol-fed rats as compared with pair-fed controls. The NADPH-dependent lipid peroxidation in liver microsomes was about 10-fold higher in microsomes from alcohol-treated rats fed corn oil as compared with controls, but only 2- to 3-fold higher in alcohol-fed rats receiving fish oil than in pair-fed controls. This was due to a higher rate of NADPH-dependent lipid peroxidation in the control rats receiving fish oil. There was a pronounced correlation between the amount of CYP2E1 and the microsomal NADPH peroxidation in variously treated rats, and between the 2E1 levels and the pathology score. The data suggest that fish oil diet, like corn oil, supports ethanol-induced liver injury which is related to CYP2E1 induction and the presence of polyunsaturated fatty acids in the diet (i.e., either n-6 or n-3).

Effects of fish and safflower oil feeding on subcellular glucose transporter distributions in rat adipocytes

Effects of fish oil feeding on glucose transport systems and cell size in rat adipocytes were examined and compared with those of safflower oil or carbohydrate feeding under isoenergy intake conditions. Glucose transport activity was assessed by measuring 3-O-methyl-D-glucose transport. The concentration of erythrocyte type glucose transporter (GLUT-1) and muscle/fat type transporter (GLUT-4) was measured by immunoblotting. The amount of each transporter in intact cells was estimated by the amount of transporter and protein of each membrane fraction and by the recovery of marker enzymes. In cells from safflower-fed rats compared with those from carbohydrate-fed rats, insulin-stimulated glucose transport activity per cell decreased to 51% after a 1-wk feeding, and cell size increase became larger with these effects and continued for at least 4 wk. At 1 wk of feeding, GLUT-1 and GLUT-4 per cell in plasma membrane from insulin-treated cells decreased to 62 and 35%, respectively, with concomitant transporter decreases in the low-density microsome fraction. In cells from high-fish oil-fed rats in which two-thirds of safflower oil was replaced by fish oil, when compared with those from safflower oil-fed rats, insulin-stimulated glucose transport activity increased 1.7-fold after 1 wk of feeding with concomitant cellular GLUT-1 and GLUT-4 increases, but its effect declined thereafter. Parallel with this time course, cell size increase was smaller after 1 wk, but this effect also declined thereafter.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of fish oil feeding on muscle metabolism during endotoxemia

The effect of fish oil feeding on muscle metabolism during endotoxemia

171. Vascular reactivity and effects of fish oil feeding in glucocorticoid hypertension in rats

171. Vascular reactivity and effects of fish oil feeding in glucocorticoid hypertension in rats

Effects of dietary omega 3 fatty acids on vascular contractility in preanoxic and postanoxic aortic rings.

Vasomotor reactivity may contribute to the pathophysiology of ischemic injury. The atherosclerotic vessel may be particularly susceptible to vasoconstriction because of the damaged endothelial layer with resultant loss of vasodilatory factors. While dietary omega 3 fatty acids have been proposed to protect against vascular occlusion, it is not clear to what extent this results from alterations in the function of platelets or from changes intrinsic to the blood vessel itself. The effects of dietary supplementation with fish oils on vascular contractility were examined in endothelialized and de-endothelialized aortic rings under pre- and postanoxic conditions. De-endothelialization was defined functionally by the loss of acetylcholine-induced vasodilation in norepinephrine-preconstricted aortic rings from rats fed normal rat chow. Three groups of rats were fed diets containing either 20% menhaden oil or 20% beef tallow, both supplemented with 3% corn oil or 23% corn oil for longer than 4 weeks. All animals received vitamin E. Under well-oxygenated conditions, de-endothelialized aortic rings from rats fed fish oil and corn oil contracted to similar extents with norepinephrine and vasopressin and less than rings from rats fed beef tallow. Endothelialized (intact) and de-endothelialized rings from rats fed fish oil relaxed more in response to acetylcholine than rings from rats fed beef tallow and corn oil. After anoxic exposure and reoxygenation, KCl-induced contraction of intact rings from rats fed fish oil and corn oil was similar and less than rings from rats fed beef tallow. Intact and de-endothelialized rings from rats fed fish oil relaxed more to acetylcholine than did rings from rats fed beef tallow and corn oil. Under preanoxic or postanoxic conditions, rings from rats fed fish oil and corn oil contracted less than rings from rats fed beef tallow. The relaxation response to acetylcholine, however, was greater in rings from rats fed fish oil than from rats fed either corn oil or beef tallow. These vascular effects of fish oil feeding may result in increased blood flow to ischemic and reperfused tissues in vivo.

Metabolic effects of coconut, safflower, or menhaden oil feeding in lean and obese Zucker rats

The aim of the present investigation was to study the effects of fish oil feeding in obese Zucker rats to establish its suitability as an animal model of hyperlipidaemia, and to understand the possible mechanism of fish oil-induced perturbations in cell metabolism. Lean and obese Zucker rats were fed on diets containing 180 g coconut, safflower, or menhaden oil/kg for 10 weeks. Body-weights and food intakes of lean coconut (LC), safflower (LS), and menhaden (LM) groups were similar. Obese menhaden (OM) rats had lower food intakes and body-weights compared with obese coconut (OC) and obese safflower (OS) groups, but values for all obese rats were higher than those for lean rats. Liver weights were higher in obese compared with lean rats, but on a percentage body-weight basis menhaden oil rats had higher values within genotype. Serum cholesterol and triacylglycerol levels were lower in the OM group compared with the OC and OS groups, and in the LM group compared with the LC group. Glucose and insulin levels were highest in OS rats followed by OC and OM rats and then the lean rats. Serum triiodothyronine and thyroxine were lower in OM rats compared with OC and OS rats. Liver mitochondrial state 3 rates with glutamate-malate and succinate were lower; mitochondrial beta-oxidation was unaffected and peroxisomal beta-oxidation was higher in menhaden oil rats compared with both coconut and safflower oil rats. In general, consumption of menhaden oil lowered hepatic malic enzyme (EC 1.1.1.38, 1.1.1.40), glucose-6-phosphate dehydrogenase (EC 1.1.1.49) and glutathione peroxidase (EC 1.11.1.9) activities and elevated long-chain fatty acyl-CoA hydrolase (EC 3.1.2.2) activity when compared with the two other diets. It is concluded that obese Zucker rats do respond like human subjects to fish oil feeding but not to vegetable oils. The hypolipidaemic effect of fish oil appears to be mediated through a lowering of lipogenic enzymes, glucose-6-phosphate dehydrogenase and malic enzyme.

171. Vascular reactivity and effects of fish oil feeding in glucocorticoid hypertension in rats

171. Vascular reactivity and effects of fish oil feeding in glucocorticoid hypertension in rats

Comparative effects of dietary fish oil and carbohydrate on plasma lipids and hepatic activities of phosphatidate phosphohydrolase, diacylglycerol acyltransferase and neutral lipase activities in the rat

In rats fed a fish oil-enriched diet, plasma triacylglycerols were lowered 51%. At the same time there was a mean 45% reduction in Mg 2+-dependent phosphatidate phosphohydrolase activity in liver microsomes and a mean 20% decrease in microsomal triacylglycerol (neutral) and diacylglycerol hydrolase activities, but not of diacylglycerol acyltransferase. These observations support the hypothesis that decreases in the activities of phosphatidate phosphohydrolase and of both lipases are involved in the expression of the inhibitory effects of fish oil feeding on hepatic lipoprotein triacylglycerol secretion. Conversely, the feeding of a sucrose-enriched diet resulted in a mean 39% rise in plasma triacylglycerols, a 19% increase in triacylglycerol hydrolase and a mean 45% increase in Mg 2+-dependent microsomal phosphohydrolase activity. The effects of the two nutritional interventions on phosphatidate phosphohydrolase activity confirm a key function for this enzyme in triacylglycerol formation.