Hydrogenated Coconut Oil Diet Research Articles

Borage oil restores acidic skin pH by up-regulating the activity or expression of filaggrin and enzymes involved in epidermal lactate, free fatty acid, and acidic free amino acid metabolism in essential fatty acid-deficient Guinea pigs

Borage oil (BO) reverses a disrupted epidermal lipid barrier and hyperproliferation in essential fatty acid deficiency (EFAD). However, little is known about its effect on skin pH, which is maintained by epidermal lactate, free fatty acids (FFAs), and free amino acids (FAAs) which is generated by lactate dehydrogenase (LDH), secreted phospholipase A2 (sPLA2), or filaggrin degradation with peptidylarginine deiminase-3 (PADI3). We hypothesized that BO restores skin pH by regulating epidermal lactate, FFA metabolism, or FAA metabolism in EFAD. To test this hypothesis, EFAD was induced in guinea pigs by a hydrogenated coconut oil (HCO) diet for 8 weeks, followed by 2 weeks of a BO diet (group HCO + BO). As controls, groups HCO and BO were fed HCO or BO diets for 10 weeks. In group HCO + BO, skin pH, which was less acidic in group HCO, was restored; and epidermal lactate and total FFAs, including palmitate, stearate, linoleate, arachidate, behenate, and lignocerate, were higher than in group HCO. LDH and sPLA2 (mainly the PLA2G2F isoform) activities and protein expressions were similar between groups HCO + BO and BO. Epidermal acidic FAAs, as well as filaggrin and PADI3 protein and mRNA expressions were higher in group HCO + BO than in group HCO. Oleate, total FAAs including other FAAs, and LDH and sPLA2 mRNA expressions were not altered between groups HCO and HCO + BO. Basic FAAs were not altered among groups. Dietary BO restored acidic skin pH and increased epidermal levels of lactate, most FFAs, and acidic FAAs by up-regulating LDH, sPLA2, filaggrin, and PADI3 activities as well as protein or mRNA expressions in EFAD.

Purified fish oil eliminating linoleic and alpha linolenic acid meets essential fatty acid requirements in rats

This study examined whether purified fish oil (PFO) supplemented to an essential fatty acid deficient (EFAD) diet meets EFA needs in rats. The EFAD diet contained 10% hydrogenated coconut oil (HCO). A similar diet contained 7% HCO and 3% PFO which also provided 2.84% arachidonic acid (AA), 52.50% eicosapentaenoic acid (EPA) and 35.73% docosahexaenoic acid (DHA) but no linoleic acid (LA) or alpha linolenic acid (ALA). A 10% soybean oil control diet provided ample LA and ALA. After 4 weeks of feeding, blood glucose, plasma triglyceride and phospholipid fatty acid profiles, C-reactive protein (CRP), TNF and IL-6 were determined after saline or LPS injection. EFAD developed with the HCO diet with triene:tetraene ratios in plasma phospholipids >.20, which remained <.02 with the control and HCO+PFO diets. Mead acid levels significantly increased by a factor of 10 with the HCO diet compared to the AIN and HCO+PFO diets and were significantly lowest with the HCO+PFO diet. 18:1 n9 levels were significantly higher in plasma phospholipids and triglycerides with the HCO diet. CRP levels were significantly highest with the control diet and significantly lowest with the HCO diet. LPS significantly increased 18:1n9 and cytokines, and decreased AA and plasma glucose in all diets and significantly increased plasma triglycerides and decreased plasma glucose in controls. Providing AA, EPA and DHA in EFAD prevents EFAD over the short-term as reflected in Mead acid production, triene:tetraene ratio, and de novo lipogenesis and may reduce the inflammatory response to LPS.

Early development of essential fatty acid deficiency in rats: Fat-free vs. hydrogenated coconut oil diet

This study examined the effects of feeding an essential fatty acid deficient (EFAD) diet either without fat or with added hydrogenated coconut oil (HCO) on fatty acid profiles in rats. Both diets induced equivalent biochemical evidence of EFAD reflected by the triene/tetraene ratio in plasma phospholipids within 2 weeks. However, the HCO diet led to larger increases of 16:1n7 and 18:1n9 in muscle but smaller increases in fat tissue and plasma triglycerides than the fat-free diet, suggesting greater increases in hepatic de novo lipogenesis with the latter. In addition, the HCO diet led to larger decreases of some 18:3n3 metabolites, particularly 22:6n3, in muscle, fat and brain tissues than the fat-free diet, presumably related to lesser stimulation of elongation and desaturation. Thus, these secondary effects of an EFAD diet on fatty acid metabolism can be modified by the saturated fat in the diet while the primary impact of both diets on development of EFAD is unaffected.

Lipodystrophic and Lipo-Peroxidative Effects of Hydrogenated Coconut Oil Diet in Rats

2 Abstract: The effects of dietary saturated fat on blood lipid and lipoprotein composition and lipid peroxidation were studied in rats. Male albino rats (Rattus norvegicus) were maintained either on diets with 5% fa t supplements made of 5% soyabean oil or 5% coconut oil. Similarly, two other groups were fed diets that were isocaloric with the former but contained 25% fat supplements made of 25% soyabean oil or 25 % coconut oil. The concentration of triacylglycerols in the plasma of the high coconut oil fed rats was three to six-times those of the others. The concentration of free cholesterol was much higher in the plasma of the coconut oil-fed rats. There were significant decreases in the plasma level of chylomirons, VLDL and HDL, but a significant increase in the LDL level of the coconut oil-fed rats. In all the tissues studied, the malondialdehyde level increased significantly in the coconut oil fed rats and most prominently in the liver and the kidney, while the reduced glutathione levels decreased significantly in the coconut oil-fed rats. It i s considered that ingestion of coconut oil for a considerably long time may affect lipid metabolism and alter the structure and function of the enzymes responsible for converting the essential fatty acids to prostaglandins or their endoperoxide precursors. The increase in the malondialdehyde level and the decrease in the reduced glutathione level are indications of the lipid peroxidative effect of saturated fat diet, while the reduced HDL and high level of LDL can be major contributory factors to atherogenesis.

Comparative Effect of Gromwell (Lithospermum erythrorhizon) Extract and Borage Oil on Reversing Epidermal Hyperproliferation in Guinea Pigs

To compare the systemic efficacy of borage oil (Borago officinalis: BO) and gromwell (Lithospermum erythrorhizon), two plant species of the Boraginaceae family, epidermal hyperproliferation was induced in guinea pigs by a hydrogenated coconut oil diet for 8 weeks. Subsequently, guinea pigs were fed diets of BO (group HBO), organic extract (group HGO), or water extract (group HGW) of gromwell for 2 weeks. In groups HGO and HGW, proliferation scores and the level of ceramides, the major lipid maintaining epidermal barrier, were similar with those in normal control group BO fed BO diet for 10 weeks. Despite accumulation of 15-hydroxyeicosatrienoic acid (15-HETrE), the potent anti-proliferative metabolite of gamma-linolenic acid (GLA: major polyunsaturated fatty acid in BO), the reversal of epidermal hyperproliferation and the ceramide level of group HBO were less than those of groups HGO and HGW. Taken together, our data demonstrate that gromwell is more effective in reversing epidermal hyperproliferation with a marked increase in ceramides.

Changes in the immune functions and susceptibility to Listeria monocytogenes infection in mice fed dietary lipids.

The direct examination of the effects that fish oil diets (composed of long-chain n-3 polyunsaturated fatty acids) exert on immune system function indicates a reduction of host natural resistance to infectious diseases mainly because of a suppression of immune function generated by the fatty acids contained in this diet. Here, we evaluated the concentration of IL-12, IL-4, prostaglandin E2 and leukotriene B4 in the serum from BALB/c mice receiving four different diets. Each group was fed a diet that differed only in the source of fat: a low-fat diet (2.5% by weight), an olive oil diet (20% by weight), a fish oil diet (20% by weight) or a hydrogenated coconut oil diet (20% by weight). Mice were fed for 4 weeks and then infected with the intracellular pathogen Listeria monocytogenes. An initial reduction in the Th1-type response as a result of a decrease in IL-12p70 secretion, an inefficient action of IL-4 (Th2-type response) and no modification of pro-inflammatory lipid-mediator production could be, at least in part, the key events responsible for the inadequate elimination of L. monocytogenes from the spleens of mice fed a fish oil diet. Furthermore, our results suggest that the type of dietary lipids may affect the circulating concentration of IL-12p70 and IL-4, leading to a modulation in the protective cellular immune response to L. monocytogenes infection.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes.

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

Determination of natural resistance of mice fed dietary lipids to experimental infection induced by Listeria monocytogenes

Current understanding based on the effect of dietary lipid manipulation upon immune system function indicates that fatty acids are involved in the modulation of the immune response through different and complex pathways. Reduction of several immune parameters by fatty acid action may be applied in the treatment of diseases characterised by an overactivation of the immune system. As a consequence, a reduction of host resistance against infectious agents has been reported in animals fed dietary lipids. The present study confirms the action of dietary lipids on the survival of mice infected with the pathogenic bacterium Listeria monocytogenes. A significant increase in peritoneal cells from mice fed a hydrogenated coconut oil diet was found, while a significant reduction of bacterial recovery from spleens of these mice was observed in this group. In addition, both eicosanoid and phospholipase inhibitors did not promote any modification of lymphocyte proliferation from mice fed olive oil or fish oil.

The effect of essential fatty acid deficiency on the fatty acid composition of different salivary glands and saliva in rats

The main purpose was to compare the changes in fatty acid composition of lipids induced by essential fatty acid (EFA) deficiency in the rat submandibular, parotid and sublingual glands. Three groups of rats were fed for 28 weeks (1 week gestation, 3 weeks lactation and 24 weeks thereafter) diets containing 7% hydrogenated coconut oil (HCO) (EFA-deficient in both n-6 and n-3), 7% soybean oil (SBO) (control) and 7% safflower oil (SFO) (deficient in n-3). Rats were killed and salivary glands were dissected out. Lipids were extracted and the fatty acid composition of total lipids and phospholipids was determined by gas chromatography-mass spectrometry. The fatty-acid compositional changes indicative of an EFA deficiency, such as decreases in the levels of 18:2 n-6, along with an accumulation of 20:3 n-9, were generally observed in all the salivary glands of rats fed 7% HCO diet. In the submandibular glands, the proportions of 16:1, 18:1 n-9 and 18:1 n-7 were also higher iin the HCO-fed group than in the other two groups. There were some differences in the fatty acid composition of the three glands. Total lipids of parotid gland had higher levels of 12:0 and 18:1 n-9 as compared to the other two glands. The levels of 18:0, 20:3 n-9, 20:3 n-6 and 20:4 n-6 were, however, lower in the parotid gland as compared with the other glands. In total phospholipids of rats fed SBO- and SFO-containing diets, the sublingual gland had lower levels of 18:2 n-6 and higher levels of 20:4 n-6 than the paratid or the submandibular. These differences in fatty acid composition may be related to possible differences in chain elongation/desaturation. The changes in fatty acid composition were also reflected in total lipids of plasma, liver and whole saliva of rats fed the various diets. A number of fatty acids were identified in saliva by gas chromatography-mass spectrometry.

The influence of dietary fatty acids on the activity and metabolic control of peroxisomal carnitine palmitoyltransferase in the liver

Peroxisomes play an important role in the β-oxidation of fatty acids and they possess a membrane-bound carnitine palmitoyltransferase (CPT). Whether this enzyme is regulated by the amount and type of fat consumed in the diet has not been investigated. Therefore weanling male Lewis rats were fed for various times (2 days to 4 weeks) on a low-fat (2.5% w/w) diet (LF) or on high-fat diets containing 20% (w/w) of either hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Hepatic peroxisomal CPT activity and sensitivity to inhibition by malonyl CoA were examined. In general, feeding the high-fat diets resulted in higher CPT activity per mg peroxisomal protein (specific activity) and per g liver (capacity) than feeding the LF diet throughout the 4 week feeding period. The most rapid induction of CPT specific was seen in the livers of animals fed the SO, EPO and MO diets. Induction of CPT specific activity was maximal after one week of feeding each of the diets. Feeding the MO diet resulted in the highest CPT specific activity at most time points examined and the highest CPT capacity at all time points. In relation to feeding the LF diet, the HCO and EPO diets increased CPT specific activity and capacity by approximately 2-fold while the OO, SO and MO diets increased the CPT specific activity by 3- to 4-fold; these diets increased CPT capacity by 3.5-fold (OO), 4.5-fold (SO) and 7.4-fold (MO). These observations are consistent with previous observations that dietary fish oils increase peroxisomal β-oxidation. Peroxisomal CPT from animals fed the LF diet was the most sensitive to inhibition by malonyl CoA at each time point ([I 50] = approx. 0.5 μM). Each of the high-fat diets decreased the sensitivity of peroxisomal CPT to inhibition by malonyl CoA. The decrease in sensitivity was apparent after feeding the OO, SO or MO diets for 2 days. At all time points peroxisomal CPT from MO-fed rats was the least sensitive to malonyl CoA inhibition. At its least sensitive (after 7 days of feeding) peroxisomal CPT from MO-fed rats required a 5.7-fold higher malonyl CoA concentration to induce 50% inhibition than did the enzyme from LF-fed rats. These data indicate that both the level of fat in the diet and the fatty acid composition of high-fat diets influence CPT activity and its sensitivity to the inhibitor malonyl CoA.

Effects of Dietary Lipid Manipulation upon Graft vs Host and Host vs Graff Responses in the Rat

The popliteal lymph node (PLN) assay was used to establish whether dietary lipids with differing fatty acid compositions could affect cell-mediated immunity in the rat. Weanling rats were fed for 4 weeks on a low-fat (2.5% by weight; LF) diet or on diets containing 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO), or menhaden (fish) oil (MO). Feeding the MO diet suppressed the graft vs host response compared with feeding the LF, HCO, SO, or EPO diets, while feeding the OO diet suppressed this response compared with feeding the LF or EPO diets. Feeding the MO diet suppressed the host vs graft response compared with feeding each of the other diets. Following the graft vs host reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of LFA-1 and CD2 compared with PLN lymphocytes from animals fed the LF diet; furthermore, they had lower levels of expression of T-cell receptor (TcR), CD4, CD8, LFA-1, and CD2 compared with lymphocytes from animals fed some, and in the case of CD2 each, of the other high-fat diets, Feeding the MO diet resulted in a lower proportion of cells expressing the interleukin-2 receptor, indicating an inhibition of lymphocyte activation, and a lower proportion of CD16 +/CD3 - cells, indicating a decrease in the proportion of NK cells within the PLN. Following the host vs graft reaction, PLN lymphocytes from animals fed the MO diet had significantly lower levels of expression of TcR and CD8 compared with lymphocytes from animals fed each of the other diets; furthermore, they had lower levels of expression of CD4, CD2, and LFA-1 compared with lymphocytes from animals fed the LF, HCO, OO, or SO diets. These observations indicate that the smaller PLN size of animals fed the MO diet results from an inhibition of activation and subsequent proliferation of cells within the node and perhaps also a suppression of movement of cells from the bloodstream to the PLN, due to decreased level of expression of adhesion molecules. These lowered levels of expression might be due to an inhibitory effect of the n-3 polyunsaturated fatty acids found in MO upon components of the signal transduction pathways involved in lymphocyte activation or upon expression of the genes for the surface molecules or both.

The effects of dietary lipid manipulation on the production of murine T cell-derived cytokines.

Lymphocytes play an important part in the development and progression of a number of autoimmune and inflammatory disorders, which are characterized by the presence of activated T cells and cytokines at the site of tissue injury and in the circulation. There has been considerable interest in using dietary polyunsaturated fatty acids (PUFA), particularly the n-3 PUFA found in fish oils, in the therapy of these conditions; such therapies aim, primarily, to suppress T-lymphocyte activity. While several studies have investigated the effects of fatty acids on the production of monocyte- and macrophage-derived cytokines, few have investigated their effects on the production of T cell-derived cytokines. Each of these studies have been restricted to IL-2 and have produced results which are not entirely clear. Moreover, there have been no studies to investigate the effects of dietary lipids other than fish oils on IL-2 production or the effects of dietary lipids on lymphokines other than IL-2. To investigate the effects of dietary lipid manipulation on the production of IL-2, IL-4, IL-10 and IFN-gamma by lymphocytes, mice were fed for 8 weeks on a low fat (LF) diet or one of 4 high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO) or menhaden oil (MO). Culture medium of lymphocytes from mice fed the OO or SO diets contained significantly more IL-2 than that of lymphocytes from mice fed the LF or HCO diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Dietary Lipid Manipulation upon Inflammatory Mediator Production by Murine Macrophages

This study investigated the effects of feeding mice lipids with different fatty acid compositions upon the ability of stimulated macrophages to produce inflammatory mediators. Weanling mice were fed for 8 weeks on a low-fat (LF; 2.5% by weight) diet or on diets containing 20% by weight of hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), or menhaden (fish) oil (MO). Thioglycollate-elicited peritoneal macrophages were isolated. Macrophages isolated from MO-fed mice produced less PGE2, 6-keto-PGF1a, TXB2, and interleukin-6 in response to lipopolysaccharide (LPS) stimulation than those from mice fed each of the other diets. Macrophages from mice fed the OO, SO, or MO diets produced less tumor necrosis factor a in response to LPS stimulation than those from mice fed the LF or HCO diets. There was no effect of dietary lipid manipulation upon the production of interleukin-1 by LPS-stimulated macrophages. Macrophages from mice fed the MO diet produced more superoxide and hydrogen peroxide in response to phorbol ester stimulation than those from mice fed each of the other diets. In response to unopsonized zymosan, macrophages from mice fed the SO or MO diets produced more hydrogen peroxide than macrophages from mice fed the other diets. LPS-stimulated nitric oxide production was greater from macrophages from OO-, SO-, or MO- fed mice than from those fed the LF or HCO diets. Thus, the nature of the lipid consumed in the diet has significant effects upon the production of a variety of inflammatory mediators by macrophages. The most potent effect is caused by fish oil consumption. Possible mechanisms by which dietary fatty acids, particularly the n-3 polyunsaturated fatty acids found in fish oils, could affect mediator production by macrophages are described. The clinical relevance of such effects is discussed.

Comparison of the effects of a range of dietary lipids upon serum and tissue lipid composition in the rat

Since the type of fat consumed in the diet may play a role in the development of several disorders, it is important to ascertain the effects of different dietary fats upon parameters such as serum lipid levels and adipose deposition. The aim of this study was to determine the effects of feeding rats a range of fats with differing fatty acid compositions. Weanling male rats were fed for 10 weeks on a low fat (LF) diet or on one of five high fat diets, which contained 20% by weight of either hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Food intake, animal growth, tissue weights at sacrifice, serum and liver lipid concentrations and serum, heart, brain and adipose tissue fatty acid compositions were studied. The food intake of the LF-fed animals was greater than that of animals fed on the high fat diets; there were no differences in food intake between animals fed the high fat diets. The total energy intake was lower for animals fed on the HCO diet than for those fed on the LF, OO, EPO or MO diets; there were no other differences in energy intake between the groups. Animals fed the different diets had almost identical rates of weight gain up to 5 weeks; after this period of rapid growth, the increase in weight was slower in all groups but especially in the LF-fed animals. The LF-fed rats had a lower total weight gain and smaller final weights than rats fed on the high fat diets. Animals fed on the MO diet had a greater weight gain than those fed on the OO or EPO diets and their final weights were greater. The MO diet resulted in greatly increased liver weight compared with each of the other diets. The HCO, OO and EPO diets also increased liver weight compared with the LF diet. The total lipid content of the livers from rats fed the high fat diets was greater than that of those from rats fed the LF diet; the livers from animals fed the MO diet contained more lipid than those from animals fed each of the other diets. MO feeding increased the free cholesterol, cholesterol ester and triacylglycerol contents of the liver. Each of the high fat diets resulted in an increase in epididymal fat pad weight compared with the LF diet, but the high fat diets resulted in different degrees of adipose deposition; the EPO and MO diets resulted in smaller epididymal fat pads than the HCO, OO and SO diets. Serum total cholesterol concentrations were higher after feeding the OO, SO or EPO diets than after feeding the LF or MO diets. The MO diet resulted in a total serum cholesterol concentration which was lower than that of animals fed each of the other diets. The serum cholesterol ester concentration of the MO-fed animals was lower than that of the LF-, SO- or EPO-fed animals. Serum triacylglycerol concentrations of the HCO- and OO-fed rats were higher than those of the LF-, SO-, EPO- or MO-fed animals. The fatty acid compositions of the serum, adipose tissue and the neutral lipid and phospholipid fractions of the heart reflected those of the diets themselves, apart from those from the HCO-fed animals, which contained much lower proportions of medium chain fatty acids than did the diet. The fatty acid composition of the phospholipid fraction of the brain was not affected by dietary lipid manipulation. The fatty acid composition of the diet affects animal growth, tissue weights, serum cholesterol, cholesterol ester and triacylglycerol concentrations and the fatty acid compositions of the serum, adipose tissue and heart. The fatty acid composition of the brain is relatively resistant to dietary modification.

The effect of fatty acids on leucocyte subsets and proliferation in rat whole blood

Polyunsaturated fatty acids (PUFA) have been shown to suppress immune cell functions in vitro. Dietary studies investigating the effects of PUFA-containing oils on lymphocyte functions have yielded contradictory findings; such studies are difficult to compare since there are many variations in protocols. The present study investigated the effects of exogenously added fatty acids on proliferation of leucocytes to whole blood in vitro and the effects of feeding diets containing oils rich in saturated fatty acids, monounsaturated fatty acids, n-6 PUFA or n-3 PUFA on rat leucocyte proliferation in whole blood and on receptor and surface marker expression by peripheral blood leucocytes. When added exogenously to whole blood all fatty acids tested, except myristic acid, inhibited leucocyte proliferation; the greatest inhibition of proliferation was seen with arachidonic and eicosapentaenoic acids. To investigate the effects of dietary lipids on proliferation and surface marker expression by leucocytes, rats were fed for ten weeks on a low fat (LF) diet (approximately 2% fat by weight) or on one of five high fat diets, which contained 20% (by weight) hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Compared with feeding the LF, SO or EPO diets, the HCO, OO and MO diets suppressed the proliferation of leucocytes in whole blood at low concentrations of Con A. High fat feeding decreased the sensitivity of B-cells to LPS, but had no effect on the magnitude of the response to this mitogen. Dietary lipid manipulation had no effect on leucocyte subpopulations (T-cells, B-cells, CD4 + cells, CD8 + cells, monocytes/macrophages, natural killer cells) or on the expression of adhesion molecules (LFA-1, ICAM, CD2). The effects of dietary lipid manipulation on leucocyte proliferation are clearly very different from the effects of addition of single fatty acids to whole blood in vitro. This is likely to be due to alterations in blood triacylglycerol and cholesterol concentrations brought about by different dietary lipids, suggesting that dietary lipids have marked effects on leucocyte proliferation and that the use of the whole blood system may be a more physiological way of determining the effects of dietary lipids on immune function than the use of single exogenously added fatty acids with purified cells.

Effects of Dietary Lipid Manipulation upon Rat Spleen Lymphocyte Functions and the Expression of Lymphocyte Surface Molecules

Rats were fed for 12 weeks on a low fat (LF; 2.5% by weight) diet or on one of five high fat (20% by weight) diets; the latter contained hydrogenated coconut oil (HCO), olive oil (OO), safflower oil (SO), evening primrose oil (EPO) or menhaden (fish) oil (MO). Feeding the EPO or MO diets resulted in inhibition of mitogen-stimulated spleen lymphocyte proliferation compared with feeding any of the other diets; in addition, feeding the OO diet resulted in inhibition of proliferation compared with feeding the LF diet. Feeding the OO, EPO or MO diets resulted in inhibition of spleen lymphocyte natural killer (NK) cell activity compared with feeding the LF or HCO diets; feeding the SO diet resulted in inhibition of NK cell activity compared with feeding the HCO diet. There was no effect of dietary lipid manipulation upon the proportion of T-cells or of CD4+ or CD8+ cells in the spleen. The level of expression of CD2 on CD4+ and CD8+ spleen lymphocytes was decreased by MO feeding compared with feeding the LF, HCO, SO or EPO diets; OO feeding decreased the level of expression of CD2 on CD4+ spleen lymphocytes compared with feeding the LF diet. The level of expression of LFA-1 was decreased on both CD4+ and CD8+ spleen lymphocytes from animals fed the OO or MO diets compared with that on lymphocytes from animals fed some of the other diets. Following mitogenic stimulation the level of expression of CD8, CD2, ICAM-1, LFA-1 and the interleukin-2 receptor was lower on spleen lymphocytes from animals fed the MO diet and, for some of the markers, on those from animals fed the OO or EPO diets. These observations indicate that diets containing MO, OO and EPO exert immunomodulatory effects by influencing the expression of important molecules upon the lymphocyte surface. This may occur through effects on signal transduction pathways and/or gene expression.

Dietary protein deficiency affects n−3 and n−6 polyunsaturated fatty acids hepatic storage and very low density lipoprotein transport in rats on different diets

Fatty livers and the similarity between the skin lesions in kwashiorkor and those described in experimental essential fatty acid (EFA) deficiency have led to the hypothesis that protein and EFA deficiencies may both occur in chronic malnutrition. The relationship between serum very low density lipoprotein (VLDL) and hepatic lipid composition was studied after 28 d of protein depletion to determine the interactions between dietary protein levels and EFA availability. Rats were fed purified diets containing 20 or 2% casein and 5% fat as either soybean oil rich in EFA, or salmon oil rich in eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids, or hydrogenated coconut oil poor in EFA. Animals were divided into six groups, SOC (20% casein + 5% soybean oil), SOd (2% casein + 5% soybean oil), COC (20% casein + 5% hydrogenated coconut oil), COd (2% casein + 5% hydrogenated coconut oil), SAC (20% casein + 5% salmon oil) and SAd (2% casein + 5% salmon oil). After 28 d, liver steatosis and reduced VLDL-phospholipid contents (P < 0.001) were observed in protein-deficient rats. In protein deficiency, triacylglycerol and phospholipid fatty acid compositions in both liver and VLDL showed a decreased polyunsaturated-to-saturated fatty acid ratio. This ratio was higher with the salmon oil diets and lower with the hydrogenated coconut oil diets. Furthermore, independent of the oil in the diet, protein deficiency decreased linoleic and arachidonic acids in VLDL phospholipids. Conversely, despite decreased proportions of EPA at low protein levels, DHA levels remained higher in rats fed salmon oil diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Glucose homeostasis in thyroxine-treated BHE/cdb rats fed corn oil or hydrogenated coconut oil

Glucose turnover was assessed in BHE rats fed either a 6% corn or hydrogenated coconut oil diet and treated with 10 μg thyroxine (T 4/100 g body weight/day or untreated. Regardless of fat souce, measures of fractional irreversible glucose turnover and Cori cycle activity were higher in T 4-treated rats than in control rats. T 4 also increased the alanine to glucose conversion. Treatment with T 4 resulted in less muscle and hepatic glycogen. Lipogenesis was greatly increased in the rats fed hydrogenated coconut oil and this effect was potentiated by T 4 treatment. Blood glucose levels were also lower in this group, suggesting that this blood glucose lowering was due to a combination of treatment effects on glycogenolysis and lipogenesis. It would appear that the main effect of T 4 was to alter the sources of glucose in the total glucose pool in the body, and that the differences in glucose oxidation, synthesis, and recycling were a reflection of the body's adaptation to this reduction.

Hyperthyroidism in BHE/cdb rats does not induce an increase in mitochondrial respiration

The effects of thyroxine (T 4) treatment and hydrogenated coconut oil (HCO) feeding on mitochondrial metabolism were studied in BHE/cdb rats. BHE/cdb rats were fed either a 6% corn oil (CO) or HCO diet for 4 weeks and injected with 10μg T 4/day/100 g body weight during the last week. Hyperthyroidism was confirmed by measuring serum hormone levels and the activity of Ca ++, Mg ++ ATPase, and the α glycerophosphate shuttle. All were significantly elevated. Respiration supported by succinate, β-hydroxybutyrate, pyruvate plus malate, α ketoglutarate, palmitoyl CoA, palmitoyl carnitine, octanoyl CoA, and octanoyl carnitine was determined. With the TCA cycle intermediate, T 4 failed to induce an increase in state 3 respiration despite having an effect on shuttle and ATPase activity. There was no effect of diet or T 4 on the transition temperatures or on the upper or lower activation energies of succinate-supported respiration. The lack of a T 4 effect on respiration supported by the TCA cycle intermediates suggests a strain-specific aberration in the responsiveness of the mitochondrial respiratory chain to T 4 induction. This suggests that this treatment might be a powerful tool to probe the role of mitochondrial dysfunction in the progressive development of the abnormal glucose tolerance in BHE/cdb rats as they age.

Effect of n-3 and n-6 fatty acids on hepatic microsomal lipid metabolism: a time course study.

The present study examines the time dependent effects of n-6 and n-3 polyunsaturated fatty acids on liver microsomal lipid metabolism in FVB mice fed a diet supplemented with a mixture of free fatty acids (mainly 18:3n-6 and 20:5n-3) at 25 mg/g diet. Significant changes in the fatty acid composition of total liver and microsomal lipids were observed after 7 days on the diets. Thereafter, some animals remained on the same diet while others were fed a diet supplemented with hydrogenated coconut oil (HCO). With the exception of 20:5n-3 which showed a slower recovery, establishment of the HCO pattern was rapid indicating that the diet-induced changes could be easily reversed. The unsaturation index, the cholesterol/phospholipid ratio and the microviscosity of the microsomal membranes were not affected by these dietary manipulations. Unsaturated fatty acid supplementation reduced the activity of delta 9 desaturase by 50%. Feeding the HCO diet to mice previously fed the EPA/GLA diet led to a progressive increase in delta 9 desaturase activity, reaching 80% of the day zero values after 14 days. The monoene content of hepatic total lipids reflected, in most cases, the changes in enzyme activity. This study shows that a low dose of a n-3 and n-6 free fatty acid mixture increases the quantities of members of the n-3 family, without loss of n-6 fatty acids in microsomal membranes and modifies the activity of delta 9 desaturase without altering the microsome physicochemical parameters.