Phospholipid Composition Of Liver Research Articles

Hepatic resistance to cold ferroptosis in a mammalian hibernator Syrian hamster depends on effective storage of diet-derived \u03b1-tocopherol

Mammalian hibernators endure severe and prolonged hypothermia that is lethal to non-hibernators, including humans and mice. The mechanisms responsible for the cold resistance remain poorly understood. Here, we found that hepatocytes from a mammalian hibernator, the Syrian hamster, exhibited remarkable resistance to prolonged cold culture, whereas murine hepatocytes underwent cold-induced cell death that fulfills the hallmarks of ferroptosis such as necrotic morphology, lipid peroxidation and prevention by an iron chelator. Unexpectedly, hepatocytes from Syrian hamsters exerted resistance to cold- and drug-induced ferroptosis in a diet-dependent manner, with the aid of their superior ability to retain dietary α-tocopherol (αT), a vitamin E analog, in the liver and blood compared with those of mice. The liver phospholipid composition is less susceptible to peroxidation in Syrian hamsters than in mice. Altogether, the cold resistance of the hibernator’s liver is established by the ability to utilize αT effectively to prevent lipid peroxidation and ferroptosis.

Liver phospholipids fatty acids composition in response to different types of diets in rats of both sexes

BackgroundDietary intake influence changes in fatty acids (FA) profiles in liver which plays a central role in fatty acid metabolism, triacylglycerol synthesis and energy homeostasis. We investigated the effects of 4-weeks treatment with milk- and fish-based diet, on plasma biochemical parameters and FA composition of liver phospholipids (PL) in rats of both sexes.MethodsAdult, 4 months old, Wistar rats of both sexes, were fed with different types of diets: standard, milk-based and fish-based, during 4 weeks. Analytical characterization of different foods was done. Biochemical parameters in plasma were determined. Fatty acid composition was analyzed by gas-chromatography. Statistical significance of FA levels was tested with two-way analysis of variance (ANOVA) using the sex of animals and treatment (type of diet) as factors on logarithmic or trigonometric transformed data.ResultsOur results showed that both, milk- and fish-based diet, changed the composition and ratio of rat liver phospholipids FA, in gender-specific manner. Initially present sex differences appear to be dietary modulated. Although, applied diets changed the ratio of total saturated fatty acids (SFA), monounsaturated fatty acids (MUFA) and polyunsaturated fatty acids (PUFA), and effects were gender specific. Milk-based diet lowered SFA and elevated MUFA in males and increased PUFA in females vs. standard diet. The same diet decreased n-3, increased n-6 and n-6/n-3 ratio in males. Fish-based diet increased n-3, decreased n-6 and n-6/n-3 ratio vs. standard and milk-based diet in females. However, the ratio of individual FA in liver PL was also dietary-influenced, but with gender specific manner. While in females fish-based diet decreased AA (arachidonic acid) increased level of EPA (eicosapentaenoic acid), DPA (docosapentaenoic acid) and DHA (docosahexaenoic acid), the same diet elevated only DHA levels in males.ConclusionGender related variations in FA composition of rat liver PL were observed, and results have shown that those initial differences could be significantly modulated by the type of diet. Furthermore, the modulatory effects of milk- and fish-based diets on liver phospholipids FA profiles appeared to be sex-specific.

Effects of dietary inulin on bacterial growth, short-chain fatty acid production and hepatic lipid metabolism in gnotobiotic mice

In literature, contradictory effects of dietary fibers and their fermentation products, short-chain fatty acids (SCFA), are described: On one hand, they increase satiety, but on the other hand, they provide additional energy and promote obesity development. We aimed to answer this paradox by investigating the effects of fermentable and non-fermentable fibers on obesity induced by high-fat diet in gnotobiotic C3H/HeOuJ mice colonized with a simplified human microbiota. Mice were fed a high-fat diet supplemented either with 10% cellulose (non-fermentable) or inulin (fermentable) for 6 weeks. Feeding the inulin diet resulted in an increased diet digestibility and reduced feces energy, compared to the cellulose diet with no differences in food intake, suggesting an increased intestinal energy extraction from inulin. However, we observed no increase in body fat/weight. The additional energy provided by the inulin diet led to an increased bacterial proliferation in this group. Supplementation of inulin resulted further in significantly elevated concentrations of total SCFA in cecum and portal vein plasma, with a reduced cecal acetate:propionate ratio. Hepatic expression of genes involved in lipogenesis (Fasn, Gpam) and fatty acid elongation/desaturation (Scd1, Elovl3, Elovl6, Elovl5, Fads1 and Fads2) were decreased in inulin-fed animals. Accordingly, plasma and liver phospholipid composition were changed between the different feeding groups. Concentrations of omega-3 and odd-chain fatty acids were increased in inulin-fed mice, whereas omega-6 fatty acids were reduced. Taken together, these data indicate that, during this short-term feeding, inulin has mainly positive effects on the lipid metabolism, which could cause beneficial effects during obesity development in long-term studies.

Feeding into old age: long-term effects of dietary fatty acid supplementation on tissue composition and life span in mice

Smaller mammals, such as mice, possess tissues containing more polyunsaturated fatty acids (PUFAs) than larger mammals, while at the same time live shorter lives. These relationships have been combined in the ‘membrane pacemaker hypothesis of aging’. It suggests that membrane PUFA content might determine an animal’s life span. PUFAs in general and certain long-chain PUFAs in particular, are highly prone to lipid peroxidation which brings about a high rate of reactive oxygen species (ROS) production. We hypothesized that dietary supplementation of either n-3 or n-6 PUFAs might affect (1) membrane phospholipid composition of heart and liver tissues and (2) life span of the animals due to the altered membrane composition, and subsequent effects on lipid peroxidation. Therefore, we kept female laboratory mice from the C57BL/6 strain on three diets (n-3 PUFA rich, n-6 PUFA rich, control) and assessed body weights, life span, heart, and liver phospholipid composition after the animals had died. We found that while membrane phospholipid composition clearly differed between feeding groups, life span was not directly affected. However, we were able to observe a positive correlation between monounsaturated fatty acids in cardiac muscle and life span.

Egg yolk conjugated linoleic acid alters phospholipid molecular species in chick tissues

AbstractThe effects of egg conjugated linoleic acid (CLA) on chick yolk sac and liver phospholipid composition and molecular species were determined. Fertile eggs with no (control), low (CLA1) or high (CLA2) levels of CLA were incubated. Upon hatching, total lipid in the remnant yolk sac constituted 11.5, 18.9 and 15.3% in control, CLA1 and CLA2, respectively (p <0.05). Maternal CLA led to a decrease in phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEtn) and an increase in lysophosphatidylcholine (LPtdCho) in the yolk sac and liver tissues of CLA1 and CLA2 when compared to control (p <0.05). The effect of maternal dietary CLA was very prominent in yolk sac PtdCho (34:1) where 13 and 38% reductions were observed in CLA1 and CLA2, respectively, when compared to control. Among different liver PtdCho species, the highest difference was found in 36:2, where a 41% increase was observed in CLA2 when compared with control chicks. The liver LPtdCho of CLA1 and CLA2 chicks had a 92% increase in 16:0 and 18:0 when compared to control. Over 80% increase was observed for 18:2 and 20:4 in the liver LPtdCho of CLA2 chicks compared to control. These results suggest that the yolk CLA content alters the proportions of phospholipids in the progeny during avian embryogenesis.

Glycerol-3-Phosphate Acyltransferase 1 Is Essential for the Immune Response to Infection with Coxsackievirus B3 in Mice

Livers and hearts from mice deficient in glycerol-3-phosphate acyltransferase 1 (GPAT1; Gpat1−/−) have a decreased content of glycerolipid intermediates and triacylglycerol, an altered composition of liver phospholipids, and elevated markers of oxidative stress. Compared with control C57BL/6 mice, infection of Gpat1−/− mice with coxsackievirus B3 (CVB3) resulted in higher mortality, an ∼50% increase in heart pathology, a significant increase in liver viral titers, and a 100-fold increase in heart viral titers. Moreover, heart mRNA levels for proinflammatory cytokines tumor necrosis factor-α, interleukin (IL)-6, and IL-1B were increased in the Gpat1−/− mice. Loss of Gpat1 also resulted in dysregulation of specific immune cells. Splenic dendritic cells from Gpat1−/− mice were fully capable of stimulating T cells from control mice; however, splenic T cells from Gpat1−/− mice were defective in their response to CVB3 antigen. Our data indicate that a lack of GPAT1 activity affects both innate and adaptive immune mechanisms. Innate mechanisms may be affected by altered membrane composition or host redox status, whereas the adaptive response may require GPAT1 activity itself.

Effects of dietary supplemental fish oil during the peripartum period on blood metabolites and hepatic fatty acid compositions and total triacylglycerol concentrations of multiparous Holstein cows

The objectives were to evaluate the effects of dietary fish oil on plasma metabolite, hepatic fatty acid composition, and total triacylglycerol concentrations. Multiparous Holstein cows (n=42) were completely randomized to 1 of 3 treatments at 3wk prepartum. Treatments were no supplemental lipid or supplemental lipid from either Energy Booster (Milk Specialties Co., Dundee, IL) or fish oil. Treatment diets were fed from −21d relative to expected date of parturition until 10d postpartum. Treatments were fed as a bolus before the a.m. feeding. The dose of lipid fed during the prepartum period was 250g, whereas approximately 0.92% of the previous day's dry matter intake was supplemented postpartum. Blood was collected 3 times weekly for determination of plasma metabolites. Liver biopsies were performed at 21 and 10d before expected date of parturition and 1 and 14d after parturition to determine fatty acid compositions and total triacylglycerol concentrations. Dry matter intake, milk yield, and loss of body weight or body condition score were not affected by supplementing the diet with lipid or by the source of lipid. Supplemental lipid tended to increase plasma glucose and decrease nonesterified fatty acids during the postpartum period. Furthermore, plasma β-hydroxybutyrate was reduced during the postpartum period in the lipid-supplemented treatments. However, source of supplemental lipid had no influence on any blood metabolite. Supplemental fish oil altered the fatty acid composition of liver phospholipids and triacylglycerols, decreasing total saturated fatty acids and increasing total n-3 and long-chain polyunsaturated fatty acids (>20 carbon fatty acids). Despite the altered fatty acid composition, hepatic total triacylglycerol concentrations were unaffected by supplemental fish oil. Furthermore, the improved metabolic profile following lipid supplementation did not decrease hepatic total triacylglycerol concentrations.

Impact of dietary protein on lipid metabolism in hamsters is source-dependent and associated with changes in hepatic gene expression

This study tested the hypothesis that protein source is a factor determining the impact of the diet on lipid metabolism in hamsters. Twenty-eight hamsters of similar body weight were assigned for a period of 8 weeks to one of the following four diets (seven per group) containing either 20 % (w/w) casein (CAS), beef protein (BF), wheat gluten (WG) or soya protein (SOY). The fat composition of the diet was the same (15.5 % w/w) in all groups and provided SFA, MUFA and PUFA representative of the average Canadian diet. After an overnight fast, blood and liver were collected for the measurement of serum lipids, fatty acid composition of liver phospholipids and mRNA levels of selected genes involved in lipid metabolism. WG resulted in lower total cholesterol, HDL-cholesterol and non-HDL-cholesterol but, along with SOY, in higher mRNA levels of cholesterol 7 alpha-hydroxylase and LDL receptor. Furthermore, both WG and SOY resulted in lower 18 : 3n-3, 20 : 4n-6, total n-6 PUFA, 18 : 1n-9 and total MUFA, but higher 22 : 6n-3, total n-3 PUFA, 22 : 6n-3/18 : 3n-3 and 22 : 5n-3/18 : 3n-3 ratios in liver phospholipids, and higher hepatic Delta6-desaturase mRNA levels. These results show that the impact of dietary protein on lipid metabolism is source-dependent and associated with changes in mRNA abundances of key hepatic enzymes and receptors.

Lack of GPAT1 enhances the pathology associated with coxsackievirus B3 infection in mice

The mitochondrial isoform of glycerol-3-phosphate acyltransferase (GPAT-1) has been shown to be important in the synthesis of triacylglycerol and in the placement of saturated fatty acids at the sn-1 position of phospholipids. A mouse deficient in GPAT1 (GPAT1−/ −) demonstrated altered composition of liver phospholipids and elevated oxidative stress. Previous research in our laboratory demonstrated that coxsackievirus B3 (CVB3) infection can be exacerbated by increasing the oxidative stress status of the host. To determine if a lack of GPAT1 activity would influence the host response to infection, we infected GPAT1−/ − and wildtype mice with CVB3 and killed the mice ten days later. Heart pathology was significantly increased in GPAT1−/ − mice, although viral titers were not different. Measurement of mRNA levels in the hearts of infected mice for the proinflammatory immune mediators MCP-1, MIP-1α, TNF-α, and IL-2 revealed different patterns of expression between GPAT1−/ − and wildtype mice. Because infection with CVB3 induces inflammatory heart pathology, changes in membrane composition may affect immune function, resulting in alterations in heart pathology. Taken together, these data suggest that a lack of GPAT1 alters the immune response to a viral infection, perhaps by changing host redox status and/or immune cell membrane composition, thereby altering immune function.

Polyunsaturated Fatty Acid Pattern in Liver and Erythrocyte Phospholipids from Obese Patients

Our aim was to study the fatty acid (FA) composition of liver phospholipids and its relation to that in erythrocyte membranes from patients with obese nonalcoholic fatty liver disease (NAFLD), as an indication of lipid metabolism alterations leading to steatosis. Eight control subjects who underwent antireflux surgery and 12 obese patients with NAFLD who underwent subtotal gastrectomy with a gastro-jejunal anastomosis in Roux-en-Y were studied. The oxidative stress status of patients was assessed by serum F2-isoprostanes levels (gas chromatography/negative ion chemical ionization tandem mass spectrometry). Analysis of FA composition of liver and erythrocyte phospholipids was carried out by gas-liquid chromatography. Patients with NAFLD showed serum F2-isoprostanes levels 84% higher than controls. Compared with controls, liver phospholipids from obese patients exhibited significantly 1) lower levels of 20:4n-6, 22:5n-3, 22:6n-3 [docosahexaenoic acid (DHA)], total long-chain polyunsaturated FA (LCPUFA), and total n-3 LCPUFA, 2) higher 22:5n-6 [docosapentaenoic acid (DPAn-6)] levels and n-6/n-3 LCPUFA ratios, and 3) comparable levels of n-6 LCPUFA. Levels of DHA and DPAn-6 in liver were positively correlated with those in erythrocytes (r = 0.77 and r = 0.90, respectively; p < 0.0001), whereas DHA and DPAn-6 showed a negative association in both tissues (r = -0.79, p < 0.0001 and r = -0.58, p < 0.01, respectively), associated with lower DHA/DPAn-6 ratios. Obese patients with NAFLD showed marked alterations in the polyunsaturated fatty acid pattern of the liver. These changes are significantly correlated with those found in erythrocytes, thus suggesting that erythrocyte FA composition could be a reliable indicator of derangements in liver lipid metabolism in obese patients.

Correlation between dietary polyunsaturated fatty acids and plasma homocysteine concentration in vitamin B 6-deficient rats

Vitamin B6 as cofactor of Delta6 desaturase is involved in polyunsaturated fatty acid metabolism; moreover, it is a cofactor of the trans-sulfuration pathway of homocysteine. Some studies report that low concentrations of pyridoxine, by increasing homocysteine levels, are associated with coronary artery disease, and carotid and arterial lesions. The aim of this study was to verify whether different dietary amounts of polyunsaturated fatty acids associated with low content of vitamin B6 could modulate homocysteinemia. Thirty-two rats were divided into two groups, one fed a diet with adequate vitamin B6 content the other a diet containing low amount of the same vitamin. Within each group, rats were divided into two subgroups differing in the polyunsaturated fatty acid content of the diet (63 and 33%, respectively). The vitamin B6-deficient diet induced an increase in homocysteine concentration compared to the vitamin B6-normal diet. This increase was tenfold in the subgroup fed high polyunsaturated fatty acid levels and twofold in the other subgroup. The fatty acid composition of liver phospholipids showed a lower arachidonic acid relative molar content and a lower 20:4/18:2 ratio in vitamin B6-deficient groups compared with B6-normal groups. On the basis of the different biological functions of pyridoxine and considering that some factors closely related to atherosclerosis are vitamin B(6) dependent, adequate pyridoxine availability could be necessary to assure a normal long chain fatty acid metabolism and to reduce the risk linked to hyperhomocysteinemia.

Dietary fish protein lowers blood pressure and alters tissue polyunsaturated fatty acid composition in spontaneously hypertensive rats

Objectives To investigate the effect of two types of dietary protein on blood pressure, liver fatty acid desaturation and composition, and urine 6-keto-prostaglandin-F (PGF 1α) level, the metabolite of prostacyclin. Methods 5-wk-old spontaneously hypertensive rats were fed 20% casein or purified fish protein. The fat source was 5% ISIO oil, which contains 47.9% (ω-6) and 1.7% (ω-3) total polyunsaturated fatty acids. After 2 mo on the diet, systolic blood pressure was reduced with fish protein compared with casein (189.8 ± 10.5 versus 220.7 ± 8.7). Results Excretion of 6-keto-PGF 1α in urine was negatively correlated with blood pressure. Liver cholesterol and phospholipid concentrations were 1.71- and 1.27-fold lower with fish protein than with casein, respectively. The fish protein diet lowered the 20:4(ω-6) proportion and the ratio of 20:4(ω-6) to 18:2(ω-6) in liver microsomal lipids and phospholipids, which was due to the reduced microsomal Δ6(ω-6) desaturation activity. Dietary protein source did not affect ω-3 fatty acid composition, and this was associated with a similar activation of Δ6(ω-3) desaturation in liver microsomes. Conclusions The present data indicated a significant blood pressure–lowering effect caused by fish protein, rather than by casein, that modified the fatty acid composition of liver phospholipids and liver microsomal total lipids.

The Fatty Acid Composition of Liver Phospholipids of the CowBos taurus Infected with the TrematodeOrientobilharzia turkestanica

The Fatty Acid Composition of Liver Phospholipids of the CowBos taurus Infected with the TrematodeOrientobilharzia turkestanica

Alterations of Rat Liver Phospholipid Composition Induced by Oral Thalidomide

In an attempt to elucidate the effects of oral thalidomide on liver phospholipid composition, doses of 1 and 3 mg/kg/day of thalidomide were orally administered to two groups of female Wistar rats (7 animals each), respectively, over a period of 60 days. Control animals (n = 7) received corresponding quantities of the vehicle alone. Chromatographic analysis and quantitative determination of the isolated phospholipid classes revealed statistically significant alterations of phospholipid fractions in the liver of the animals treated with the higher thalidomide dose (3 mg/kg/day). These alterations may be associated with changes in the metabolic activity, ionic transport and cell-cell interactions of the hepatic cellular components.

Effects of peroxisome proliferators on rat liver phospholipids: sphingomyelin degradation may be involved in hepatotoxic mechanism of perfluorodecanoic acid.

Perfluorooctanoic acid (PFOA), perfluorodecanoic acid (PFDA), clofibrate, di(2-ethylhexyl)phthalate (DEHP), and Wy-14,643 represent a class of compounds known as peroxisome proliferators (PPs). Such compounds induce biogenesis of liver peroxisomes and cause a varying degree of hepatotoxicity and carcinogenesis in rodents. We examined the effects of these PPs on rat hepatic lipids and phospholipid profiles using phosphorus-31 NMR spectroscopy. All PPs caused a 25-57% increase in hepatic phospholipid content, while all but clofibrate increased the total lipid content by 26-156%. Treatments also influenced the composition of liver phospholipids. Phosphatidylcholine (PtdCho) and phosphatidylethanolamine (PtdEth) contents were significantly increased in all treatment groups. Most notably, PFDA caused the largest increase in PtdCho and PtdEth content (ca. 70%), while PFOA and Wy-14,643 were the only test compounds that influenced the PtdCho:PtdEth ratio. PFDA also caused an ca. 30% decrease in sphingomyelin (SphM) from 24 to 120 h postdose. SphM is a key lipid in signal transduction processes involved in apoptosis. Hydrolysis of SphM can be mediated through the action of tumor necrosis factor (TNF-alpha). We measured the TNF-alpha concentrations in rat sera at 24 h post-PFDA-exposure and found an 8-fold increase relative to vehicle-treated controls. These data demonstrate that an increase in the serum TNF-alpha level correlates with the time frame for the observed reduction in hepatic SphM. PFOA, a structurally similar compound, had no effect on hepatic SphM content, nor did it affect the serum TNF-alpha concentration. These effects may be related to differences in the tumorigenicity associated with these compounds. We postulate that PFDA activates the SphM signal transduction pathway via the release of TNF-alpha. This then stimulates cytotoxic responses and processes of apoptosis and may suppress cell proliferative and mitogenic responses.

Fetal brain and liver phospholipid fatty acid composition in a guinea pig model of fetal alcohol syndrome: Effect of maternal supplementation with tuna oil

Chronic prenatal ethanol exposure may impair neurological development and function severely. We have shown previously that feeding ethanol to guinea pigs throughout pregnancy leads to decreased docosahexaenoic acid 22:6ω3) content in brain phospholipids, accompanied by impaired motor function comparable to some features of human fetal alcohol syndrome. We have tested the hypothesis that dietary supplementation of pregnant guinea pigs with 22:6ω3-enriched tuna oil may reduce the ethanol-induced deficit in 22:6ω3 accumulation into fetal brain. Guinea pigs (n = 5/ group) were maintained on chow diet either alone or supplemented with 6 gm ethanol/kg/day, ethanol, and tuna oil (0.5 gm/day; 130 mg 22:6ω3/day), or tuna oil alone both before and throughout pregnancy. Fetuses were assessed at term for brain and liver phospholipid fatty acid composition. Prenatal ethanol exposure significantly decreased fetal brain phosphatidylcholine (PC) and phosphatidylethanolamine (PE) 22:6ω3 contents and increased the PC PE ratio in fetal brain. Feeding both tuna oil and ethanol increased brain PC and PE 22:6ω3 content above control values, whereas the PC PE ratio was similar to control fetuses. Feeding tuna oil alone did not alter significantly the polyunsaturated content of fetal brain phospholipids. These feeding regimens induced markedly different changes to fetal liver phospholipid compositions compared with brain, which suggests that the effects of ethanol and/or tuna oil were tissue-specific. These results show that increased 22:6ω3 availability modified the effect of ethanol on developing fetal brain phospholipid composition. Such alterations to brain fatty acid content may potentially reduce some aspects of the harmful effects of maternal ethanol consumption on prenatal neurological development.

Soybean protein lowers serum cholesterol levels in hamsters: Effect of debittered undigested fraction

the undigested fraction (UDF) of soybean protein exerts a marked hypocholesterolemic effect in relation to soybean protein (SOY) in rats. The present study was conducted to confirm whether UDF was effective in hamsters as in rats in combination with different fat sources, either perilla oil (PER) or safflower oil (SAF). Because the hamster, unlike the rat, disliked the bitter taste of UDF, the effect of debittering UDF also was studied. Cholesterol-enriched (0.2%) diets containing 20% protein and 10% fat were fed to hamsters for 4 wk. UDF was more hypocholesterolemic than soybean protein in hamsters regardless of the dietary fat source. The ratio of high-density lipoprotein to total cholesterol essentially remained unchanged. The debittered UDF, without influencing food intake and thereby weight gain, exerted a significant hypocholesterolemic effect comparable with UDF in relation to SOY accompanying stimulation of fecal neutral and acidic steroid excretion. The fatty acid composition of liver phospholipids was influenced by the type of the dietary protein, and both UDF seemed to interfere characteristically more than SOY with the desaturation systems between linoleic acid and arachidonic acid. Thus, the debittered UDF, similar to UDF, exerted a distinct influence on the various parameters of lipid metabolism in relation to SOY.

Effects of randomization of partially hydrogenated corn oil on fatty acid and cholesterol absorption, and tissue lipid levels in rats.

Randomization of partially hydrogenated corn oil containing approximately 45% of trans octadecenoic acid only slightly, but not significantly, increased the lymphatic fatty acid absorption in rats. No effect of randomization was observed on cholesterol absorption. When rats were fed these fats at the 8.8% level (with 1.2% safflower oil) for three weeks, the concentrations of serum cholesterol, and serum and liver phospholipid were significantly higher in randomized fat than in control fat, which was composed of 9% high-oleic safflower oil and 1% palm oil. Liver cholesterol tended to be higher in randomized fat. In contrast, nonrandomized fat was not hyperlipidemic compared to control fat. Although the fatty acid composition of liver phospholipids suggested a possible interference of trans fatty acid with the metabolism of linoleic acid to arachidonic acid, there was no effect of randomization. In the two hydrogenated fat groups, trans octadecenoic acid was incorporated and distributed similarly in adipose tissue triacylglycerol. These observations indicated that randomization of partially hydrogenated fat is not beneficial to various lipid parameters in rats.

Effects of different dietary fats and proteins on cholesterol metabolism and eicosanoid production in hamsters

The present study was conducted to investigate the interaction of dietary protein, soybean protein (SOY) and casein (CAS); and fat, perilla oil (PER, α-linolenic acid) and safflower oil (SAF, linoleic acid), on cholesterol metabolism, liver fatty acid composition and splenic eicosanoid production in hamsters. Cholesterol-enriched diets (0.2%) containing 20% protein and 10% fat were given for 38 days. Neither hypocholesterolemic nor liver cholesterol-lowering effects of SOY in comparison to CAS were observed in this experiment. However, SOY stimulated fecal steroid excretion, particularly in combination with SAF. The fatty acid composition of liver phospholipids was in general not influenced by the type of dietary protein, but SOY interfered the conversion of 20:5n-3 to 22:6n-3 when fed with PER. Splenic production of leukotriene B4 was not influenced by dietary treatments whereas the production of PGE2 was significantly higher in hamsters fed SAF diets, particularly in combination with SOY. Thus, SOY in comparison to CAS has selective effects on various parameters of lipid metabolism when added in cholesterol-enriched diets.

Dietary Fat Influences the Effect of Zinc Deficiency on Liver Lipids and Fatty Acids in Rats Force-Fed Equal Quantities of Diet

Previous studies showed that zinc deficiency influences the fatty acid composition of rat tissues, but the influence of dietary fat on the effects of zinc deficiency was not considered at that time. The present study was therefore conducted to investigate the effect of zinc deficiency on lipid concentrations in the liver and on fatty acid composition of liver phospholipids in rats fed diets containing coconut oil or fish oil, using a bifactorial experimental design. To ensure an adequate food intake all rats were force-fed. The zinc-deficient rats fed the coconut oil diet developed fatty livers, whereas zinc-deficient animals fed the fish oil diet did not. The zinc-deficient rats in both dietary fat groups had lower levels of linoleic acid, arachidonic acid and total (n-6) fatty acids in the liver phospholipids, especially in the phosphatidylcholine, but greater concentrations of (n-3) fatty acids compared with zinc-adequate controls. We conjecture that zinc deficiency influences incorporation of polyunsaturated fatty acids into phosphatidylcholine. The lower levels of arachidonic acid are replaced in the zinc-deficient animals fed a coconut oil diet by docosapentaenoic and docosahexaenoic acids and in the zinc-deficient animals fed a fish oil diet by eicosapentaenoic acid. The replacement of arachidonic acid by other fatty acids in the phospholipids is likely to have implications for prostaglandin synthesis. The study shows that the type of dietary fat influences the effects of zinc deficiency on fatty acid composition and especially on lipid concentrations in the liver.