Levels Of Oleate Research Articles

Altered Toxicities of Fatty Acid Salts in Green Paramecia Cultured in Different Waters

Detergents including fatty acid salts act as surface-active agents and thus possibly damage the plasma membrane structures of aquatic organisms. Therefore, when excess, the house-used and industrial outflows of such detergents into aquatic environments may have considerable impacts on the ecosystem. In this study, we propose the use of green paramecia (Paramecium bursaria) for assessing the acute toxicity of eight fatty acid salts (Na and K salts of oleate, palmitate, laurate and myristate) under various water conditions. The Paramecium in the stationary phase were used for a toxicity assay carried out on 12-well microplates and the median lethal concentration (LC50) was determined for each fatty acid salt. In the low mineral culture medium prepared with ultra-pure water, the LC50 for each fatty acid ranged from 5.8 to 144 ppm (w/v). The toxic levels of fatty acid salts differed in the following order: laurate, myristate > or = oleate, palmitate. The toxic levels of oleate and palmitate salts were ca. 10-fold lower than those of laurate and myristate salts. When river water and local tap water instead of ultra-pure water were used for culturing, the toxic levels of all fatty acid salts were drastically lowered compared to the low mineral condition by 30- to 100-fold (198-660 ppm, w/v). Similar detoxification effect was observed when Ca or Mg was added to the low mineral culture media, indicating that the toxicity of fatty acid salts can be notably lowered as the mineral content increases. As we demonstrated that toxicities of fatty acid salts can be lowered in river water and tap water compared to the low mineral condition, some chemical substances behave differently in the different water conditions. Therefore, the use of natural waters reflecting the real environmental conditions in further collection of data on the ecotoxicity impacts of variety of chemicals is highly encouraged.

Oleate accumulation, induced by silencing of microsomal omega-6 desaturase, declines with leaf expansion in transgenic tobacco

All higher plants contain at least one microsomal omega-6 desaturase (FAD2), which inserts a double bond between the carbons 12 and 13 of monounsaturated oleic acid to generate polyunsaturated linoleic acid and controls most of the polyunsaturated lipid synthesis in plant cells. RNA interference can be used to silence endogenous genes by effective degradation of target transcripts. To investigate development-related silencing of the FAD2, fatty acid composition was analyzed in the context of leaf expansion in FAD2-silenced tobacco lines obtained by RNA interference technology. We observed that the increased oleate level in unexpanded leaves due to FAD2-silencing receded significantly in fully expanded leaves. The mechanism involved in this interesting phenomenon was investigated by analyses of individual lipid proportion, fatty acid composition of individual lipids, and FAD2 transcript level in the transgenic leaves at different expansion stages. Data revealed that the expansion-related FAD2-silencing effect was not due to rebound of FAD2 transcript, but rather probably due to chloroplast development with leaf expansion.

Moderate intake of myristic acid in sn-2 position has beneficial lipidic effects and enhances DHA of cholesteryl esters in an interventional study

Among the saturated fatty acids (SFA), myristic acid is known to be one of the most atherogenic when consumed at high levels. Our purpose was to compare the effects of two moderate intakes of myristic acid on plasma lipids in an interventional study. Twenty-five male monks without dyslipidemia were given two isocaloric diets for 5 weeks each. In diet 1, 30% of the calories came from fat (8% SFA, 0.6% myristic acid) and provided 200 mg cholesterol/day. Calories of diet 2 were 34% fat (11% SFA, 1.2% myristic acid) with the same levels of oleate, linoleate, α-linolenate and cholesterol. A baseline diet was provided before each diet. In comparison with baseline, diets 1 and 2 induced a decrease in total cholesterol, LDL-cholesterol and triglycerides ( P<.001); HDL-cholesterol was not modified and the apo A-I/apo B ratio increased ( P<.001). Plasma triglycerides were lower after diet 2 than after diet 1 whereas HDL-cholesterol was higher ( P<.05). In phospholipids, myristic acid, oleic acid, linoleic acid, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) increased after diet 2 vs. baseline ( P<.01) and diet 1 ( P<.05). Both diets were associated with an increase in α-linolenate of cholesteryl esters ( P<.05), but only diet 2 was associated with an increase in DHA of cholesteryl esters ( P<.05). In diet 2, myristic acid intake was positively correlated with myristic acid of phospholipids, and α-linolenic acid intake was correlated with α-linolenic acid of cholesteryl esters. Moderate intake (1.2% of total calories) of myristic acid has beneficial lipidic effects and enhances DHA of cholesteryl esters.

Modulation of Endosomal Cholesteryl Ester Metabolism by Membrane Cholesterol

Cells acquire cholesterol in part by endocytosis of cholesteryl ester containing lipoproteins. In endosomes and lysosomes cholesteryl ester is hydrolyzed by acidic cholesteryl ester hydrolase producing cholesterol and fatty acids. Under certain pathological conditions, however, such as in atherosclerosis, excessive levels of cholesteryl ester accumulate in lysosomes for reasons that are poorly understood. Here, we have studied endosomal and lysosomal cholesteryl ester metabolism in cultured mouse macrophages and with cell-free extracts. We show that net hydrolysis of cholesteryl ester is coupled to the transfer of cholesterol to membranes. When membrane cholesterol levels are low, absorption of cholesterol effectively drives cholesteryl ester hydrolysis. When cholesterol levels in acceptor membranes approach saturation or when cholesterol export is blocked, cholesterol is re-esterified in endosomes. These results reveal a new facet of cellular cholesterol homeostasis and provide a potential explanation for cholesteryl ester accumulation in lysosomes of atherosclerotic cells.

Lack of stearoyl-CoA desaturase 1 upregulates basal thermogenesis but causes hypothermia in a cold environment

Stearoyl-CoA desaturase (SCD) is a microsomal enzyme involved in the biosynthesis of oleate and palmitoleate. Mice with a targeted disruption of the SCD1 isoform (SCD1-/-) exhibit reduced adiposity and increased energy expenditure. To address whether the energy expenditure is attributable to increased thermogenesis, we investigated the effect of SCD1 deficiency on basal and cold-induced thermogenesis. SCD1-/- mice have increased expression of uncoupling proteins in brown adipose tissue (BAT) relative to controls. The beta3-adrenergic receptor (beta3-AR) expression was increased and the phosphorylation of cAMP response element binding protein and the protein level of peroxisome proliferator-activated receptor-gamma coactivator-1alpha were increased in the SCD1-/- mice. Both lipolysis and fatty acid oxidation were increased in the SCD1-/- mice. When exposed to 4 degrees C, SCD1-/- mice showed hypothermia, hypoglycemia, and depleted liver glycogen. High levels of dietary oleate partially compensated for the hypothermia and rescued plasma glucose and liver glycogen. These results suggest that SCD1 deficiency stimulates basal thermogenesis through the upregulation of the beta3-AR-mediated pathway and a subsequent increase in lipolysis and fatty acid oxidation in BAT. The hypothermia and hypoglycemia in cold-exposed SCD1-/- mice and the compensatory recovery by oleate indicate an important role of SCD1 gene expression in thermoregulation.

Native UCP1 Displays Simple Competitive Kinetics between the Regulators Purine Nucleotides and Fatty Acids

Elucidation of the regulation of uncoupling protein 1 (UCP1) activity in its native environment, i.e. the inner membrane of brown-fat mitochondria, has been hampered by the presence of UCP1-independent, quantitatively unresolved effects of investigated regulators on the brown-fat mitochondria themselves. Here we have utilized the availability of UCP1-ablated mice to dissect UCP1-dependent and UCP1-independent effects of regulators. Using a complex-I-linked substrate (pyruvate), we found that UCP1 can mediate a 4-fold increase in thermogenesis when stimulated with the classical positive regulator fatty acids (oleate). After demonstrating that the fatty acids act in their free form, we found that UCP1 increased fatty acid sensitivity approximately 30-fold (as compared with the 1.5-fold increase reported earlier based on nominal fatty acid values). By identifying the UCP1-mediated fraction of the response, we could conclude that the interaction between purine nucleotides (GDP) and fatty acids (oleate) unexpectedly displayed simple competitive kinetics. In GDP-inhibited mitochondria, oleate apparently acted as an activator. However, only a model in which UCP1 is inherently active (i.e."activating" fatty acids cannot be included in the model), where GDP functions as an inhibitor with a K(m) of 0.05 mm, and where oleate functions as a competitive antagonist for the GDP effect (with a K(i) of 5 nm) can fit all of the experimental data. We conclude that, when examined in its native environment, UCP1 functions as a proton (equivalent) carrier in the absence of exogenous or endogenous fatty acids.

Stearoyl-CoA Desaturase 1 Gene Expression Is Necessary for Fructose-mediated Induction of Lipogenic Gene Expression by Sterol Regulatory Element-binding Protein-1c-dependent and -independent Mechanisms

Stearoyl-CoA desaturase (SCD) synthesizes oleate necessary for the biosynthesis of triglycerides and other lipids. Mice with a targeted disruption of the SCD1 gene are deficient in tissue oleate and have reduced expression of the sterol regulatory element-binding protein (SREBP) and its target genes. The SREBP-1c isoform is a known mediator of insulin action on hepatic gene expression, but its transcriptional effects due to glucose or fructose are still unclear. We found that fructose compared with glucose is a stronger inducer of SREBP-1c and lipogenic gene expression, causing a dramatic increase in hepatic triglyceride levels. However, when fed to the SCD1-/- mice, fructose failed to induce SREBP-1 or lipogenic genes and the triglyceride levels were not increased. Instead fructose feeding caused a decrease in hepatic glycogen and plasma glucose levels. The induction of SREBP-1 and lipogenic gene expression as well as the levels of liver triglycerides, glycogen, and plasma glucose was partially restored when the fructose diet was supplemented with very high levels of oleate (20% by weight) but not with palmitate, stearate, or linoleate. Fructose in a long term feeding induced the expression of SCD1 and that of other lipogenic genes in the liver of SREBP-1c-/- mice, and a further increase in expression of these genes occurred when the fructose diet was supplemented with oleate. Our observations demonstrated that oleate produced by SCD is necessary for fructose-mediated induction of lipogenic gene expression through SREBP-1c-dependent and -independent mechanisms and suggested that SCD1 gene expression is important in lipid and carbohydrate homeostasis.

Comparison of Aflatoxin Production in Normal- and High-Oleic Backcross-Derived Peanut Lines.

The effect of the high-oleate trait of peanut on aflatoxin production was tested by comparing normal oleic lines with high-oleic backcross-derived lines. Seeds were blanched, quartered, and inoculated with Aspergillus flavus conidia, placed on moistened filter paper in petri dishes, and incubated for 8 days. In one experiment, dishes were stacked in plastic bags in a Latin square design with bags and positions in stacks as blocking variables. High-oleic lines averaged nearly twice as much aflatoxin as normal lines. Background genotype had no significant effect on aflatoxin content, and interaction between background genotype and oleate level was not detected. In a second experiment, dishes were arranged on plastic trays enclosed in plastic bags and stacked with PVC spacers between trays. Fungal growth and aflatoxin production were greater than in the first experiment. Background genotype, oleate level, and their interaction were significant. The mean of high-oleic lines was almost twice that of normal lines, but the magnitude of the difference varied with background genotype. Special care should be taken with high-oleic lines to prevent growth of Aspergillus spp. and concomitant development of aflatoxin contamination.

The safety of the use of ethyl oleate in food is supported by metabolism data in rats and clinical safety data in humans

The absorption, distribution, and excretion of radiolabeled ethyl oleate (EO) was studied in Sprague–Dawley rats after a single, peroral dose of 1.7 or 3.4 g/kg body weight and was compared with a radiolabeled triacylglycerol (TG) containing only oleic acid as the fatty acid (triolein). Both test materials were well absorbed with approximately 70–90% of the EO dose absorbed and approximately 90–100% of the TG dose absorbed. At sacrifice (72 h post-dose), tissue distribution of EO-derived radioactivity and TG-derived radioactivity was similar. The tissue with the highest concentration of radioactivity in both groups was mesenteric fat. The other organs and tissues had very low concentrations of test material-derived radioactivity. Both test materials were rapidly and extensively excreted as CO 2 with no remarkable differences between their excretion profiles. Approximately 40–70% of the administered dose for both groups was excreted as CO 2 within the first 12 h (consistent with β-oxidation of fatty acids). Fecal elimination of EO appeared to be dose-dependent. At the dose of 1.7 g/kg, 7–8% of the administered dose was eliminated in the feces. At the dose of 3.4 g/kg, approximately 20% of the administered dose was excreted in the feces. Excretion of TG-derived radiolabel in the feces was approximately 2–4% for both doses. Overall, the results demonstrate that the absorption, distribution, and excretion of radiolabeled EO is similar to that of TG providing evidence that the oleic acid moiety of EO is utilized in the body as a normal dietary TG-derived fatty acid. To confirm the expected safety of EO in humans, a total of 235 subjects participated in a 12-week trial where two levels of ethyl oleate in a milk-based beverage were investigated: 8 g/day in a single serving (approximately 0.1 g/kg) and 16 g/day taken in two divided servings (approximately 0.2 g/kg). Adverse events (AEs) were recorded throughout the 12-week trial. In addition, a brief physical exam (including vital signs and body weight), ECGs, fasting serum chemistry profile, serum lipid profile, and urinalysis were performed at baseline and after study completion. Results showed the incidence of reported AEs was similar between the EO groups and the control groups. Analysis of comprehensive laboratory data revealed no EO exposure-related, clinically significant adverse changes in laboratory parameters. These studies demonstrated that EO has a highly favorable safety profile and is well tolerated in the diet.

Effect of the high-oleic trait on roasted peanut flavor in backcross-derived breeding lines.

The high-oleic trait of peanut (Arachis hypogaea L.) has been suggested to have a positive impact on the roasted peanut sensory attribute. A series of lines derived by backcrossing the high-oleic trait into several existing cultivars were compared with their parent cultivars at locations in Florida, Georgia, North Carolina, and Texas. Breeders grew their high-oleic lines and parents in three-replicate tests at one or two locations. The Florida high-oleic line F435-2-3-B-2-1-b4-B-B-3-b3-b3-1-B was grown at each location. The test included normal- and high-oleic variants of F435, GK 7, NC 7, NC 9, Sunrunner, Tamrun 96, and Tamspan 90. Sound-mature kernel samples were roasted, ground into paste, and evaluated by a sensory panel using a 14-point flavor intensity unit (fiu) scale. Background genotype had an effect (P < 0.01) on the heritable sensory attributes roasted peanut, sweet, and bitter. Oleate level had a positive effect on roasted peanut intensity, increasing it by 0.3 fiu averaged across all seven background genotypes. However, the magnitude of improvement varied across background genotypes. The high-oleic trait had no effect or increased the intensity of the roasted peanut attribute in each background genotype. The increase was greatest in Tamrun 96 (+0.6 fiu, P < 0.05) and Spanish genotypes Tamspan 90 (+0.4 fiu, P < 0.05) and F435 (+0.4 fiu, P < 0.10). A change of 0.5 fiu or more should be perceptible to consumers. Interaction between oleate level and background genotype was detected for sweet (P < 0.10) and bitter (P < 0.01) attributes. The trait had an increasing effect on the bitter attribute only in the background genotype of Tamspan 90 (+0.7 fiu, P < 0.01). There was a nonsignificant increase in bitterness in the other Spanish background genotype, F435. Changes in bitterness in runner- and Virginia-type backgrounds were close to zero. Incorporation of the high-oleic trait into peanut cultivars is likely to improve the intensity of the roasted peanut attribute, but it may also increase the bitter attribute in Spanish genotypes.

Oleate and Linoleate Enhance the Growth-promoting Effects of Insulin-like Growth Factor-I through a Phospholipase D-dependent Pathway in Arterial Smooth Muscle Cells

Diabetes causes accelerated atherosclerosis and subsequent cardiovascular disease through mechanisms that are poorly understood. We have previously shown, using a porcine model of diabetes-accelerated atherosclerosis, that diabetes leads to an increased accumulation and proliferation of arterial smooth muscle cells in atherosclerotic lesions and that this is associated with elevated levels of plasma triglycerides. We therefore used the same model to investigate the mechanism whereby diabetes may stimulate smooth muscle cell proliferation. We show that lesions from diabetic pigs fed a cholesterol-rich diet contain abundant insulin-like growth factor-I (IGF-I), in contrast to lesions from non-diabetic pigs. Furthermore, two fatty acids common in triglycerides, oleate and linoleate, enhance the growth-promoting effects of IGF-I in smooth muscle cells isolated from these animals. These fatty acids accumulate predominantly in the membrane phospholipid pool; oleate accumulates preferentially in phosphatidylcholine and phosphatidylethanolamine, whereas linoleate is found mainly in phosphatidylethanolamine. The growth-promoting effects of oleate and linoleate depend on phospholipid hydrolysis by phospholipase D and subsequent generation of diacylglycerol. Thus, concurrent increases in levels of IGF-I and triglyceride-derived oleate and linoleate in lesions may contribute to accumulation and proliferation of smooth muscle cells and lesion progression in diabetes-accelerated atherosclerosis.

Oleoyl-CoA Is the Major de NovoProduct of Stearoyl-CoA Desaturase 1 Gene Isoform and Substrate for the Biosynthesis of the Harderian Gland 1-Alkyl-2,3-diacylglycerol

1-Alkyl-2,3-diacylglycerol (ADG) is a unique neutral lipid found in the eyeball-associated Harderian gland (HG) of the mouse and acts as a lubricant to facilitate eyelid movement. We found that the HG of the mice with a disruption in the gene for stearoyl-CoA desaturase 1 (SCD1) (SCD1-/-) is deficient in ADG. The amount of C20:1n-9, which is a major fatty acid of ADG, was reduced by greater than 90% despite normal elongase enzyme activity proposed to elongate it from C18:1n-9. HG from SCD1-/- mice exhibited high desaturase activity toward C16:0-CoA as substrate but had very low desaturase activity toward C18:0-CoA. Feeding diets containing high levels of oleate to the SCD1-/- mice did not increase the levels of C18:1n-9 or C20:1n-9 in the HG and failed to restore the ADG to the levels found in the HG of the wild-type mouse. De novo ADG synthesis as measured by the incorporation of [(3)H]glycerol and [(14)C]glucose was high in the SCD1+/+ mouse but was reduced by greater than 90% in the HG of SCD1-/- mouse. The deficiencies in the levels of ADG and C20:1n-9 were not compensated for by the expression of SCD2 and SCD3 isoforms in the HG of the SCD1-/- mouse. These observations demonstrate that SCD1-synthesized oleoyl-CoA is a major substrate required for the biosynthesis of normal levels of ADG and that the SCD isoforms present in the HG have different substrate specificity.

Targeted Disruption of Stearoyl-CoA Desaturase1 Gene in Mice Causes Atrophy of Sebaceous and Meibomian Glands and Depletion of Wax Esters in the Eyelid

Stearoyl-CoA desaturase (SCD) is a microsomal rate-limiting enzyme in the cellular synthesis of monounsaturated fatty acids (MUFA), mainly oleate (18:1) and palmitoleate (16:1), which are the major MUFA of membrane phospholipids, cholesterol esters and triglycerides. Three well-characterized isoforms of SCD, SCD1, SCD2 and SCD3, exist in mice. To investigate the physiologic functions of SCD1, we generated SCD1 null (SCD1-/-) mice. The skin and eyelid of SCD1-/- mice are deficient in triglycerides and cholesterol esters, and the eyelid also is deficient in wax esters. Furthermore, the eyelid and skin of SCD1-/- mice have higher levels of free cholesterol. SCD1-/- mice develop cutaneous abnormalities and narrow eye fissure with atrophic sebaceous and meibomian glands. Consumption of diets containing high levels of oleate, failed to restore the levels of triglycerides, cholesterol esters and wax esters in SCD1-/- mice to the levels found in the eyelid of wild-type mice. These results reveal a physiologic role of SCD in cholesterol homeostasis as well as in the de novo biosynthesis of cholesterol esters, triglycerides and wax esters required for normal skin and eyelid function.

Free fatty acids activate a vigorous Ca(2+):2H(+) antiport activity in yeast mitochondria.

The accumulation and retention of Ca(2+) by yeast mitochondria (Saccharomyces cerevisiae) mediated by ionophore ETH 129 occurs with a variable efficiency in different preparations. Ineffective Ca(2+) transport and a depressed membrane potential occur in parallel, are exacerbated in parallel by exogenous free fatty acids, and are corrected in parallel by the addition of bovine serum albumin. Bovine serum albumin is not required to develop a high membrane potential when either Ca(2+) or ETH 129 are absent, and when both are present membrane potential is restored by the addition of EGTA in a concentration-dependent manner. Respiration and swelling data indicate that the permeability transition pore does not open in yeast mitochondria that are treated with Ca(2+) and ETH 129, whereas fatty acid concentration studies and the inaction of carboxyatractyloside indicate that fatty acid-derived uncoupling does not underlie the other observations. It is concluded that yeast mitochondria contain a previously unrecognized Ca(2+):2H(+) antiporter that is highly active in the presence of free fatty acids and leads to a futile cycle of Ca(2+) accumulation and release when exogenous Ca(2+) and ETH 129 are available. It is also shown that isolated yeast mitochondria degrade their phospholipids at a relatively rapid rate. The activity responsible is also previously unrecognized. It is Ca(2+)-independent, little affected by the presence or absence of a respiratory substrate, and leads to the hydrolysis of ester linkages at both the sn-1 and sn-2 positions of the glycerophospholipids. The products of this activity, through their actions on the antiporter, explain the variable behavior of yeast mitochondria treated with Ca(2+) plus ETH 129.

Viscosity measurement and modeling of lipid-supercritical carbon dioxide mixtures

The viscosities of supercritical carbon dioxide (SC-CO 2) containing different levels of methyl oleate and oleic acid were measured with a high pressure capillary viscometer. The SC-CO 2-methyl oleate system was evaluated at 313.15, 323.15 and 333.15 K and 11.5, 13.7 and 15.5 MPa, respectively. The SC-CO 2-oleic acid system was evaluated at 313.15 K and 20.5 and 30.0 MPa and 333.15 K and 30.0 MPa. The increase in SC-CO 2 viscosity was as high as 15–20% at the maximum methyl oleate concentrations (4–5 wt%) and 6–12% at the maximum oleic acid concentrations (2–3 wt%). The increase of relative viscosity with concentration was linear. The lipid-SC-CO 2 mixtures were Newtonian. The Arrhenius equation, modified by the excess Gibbs free energy using solubility parameters of the components based on the regular solution theory, predicted the liquid phase and the fluid phase viscosities of the lipid-SC-CO 2 mixtures within ± 25% and ± 1%, respectively.

Improvement of palm oil through breeding and biotechnology

AbstractThe oil palm Elaeis guineensis is the highest oil‐yielding crop and has the potential to become the major supplier of both edible oil and renewable industrial feedstock. The oil yield from wild groves is presently less than 0.5 t/ha/y. However, through breeding and selection, the oil yield of commercial plantations could reach as much as 8 t/ha/y. New planting materials also have the capability of better oil yields with high iodine value (IV), slow height increment, and larger kernels. The oil also contains considerable amounts of carotenoids (500–700 ppm), vitamin E (600–1000 ppm), and sterols (250–620 ppm). The oil yield of another oil palm species, E. oleifera, is approximately 0.5 t/ha/y with high contents of carotenoids (700–1500 ppm), vitamin E (700–1500 ppm), and sterols (3500–4000 ppm). The above traits could be improved through breeding and biotechnology. Biotechnological efforts at the Palm Oil Institute of Malaysia are directed toward the production of oil with high IV and high monounsaturated fatty acids for edible purposes and industrial uses. Isolation and manipulation of the genes involved in the biosynthesis of fatty acids are the main focus. The aim is to increase the efficiency of conversion of palmitate (C16:0) to oleate (C18:1). Levels of palmitate and oleate are controlled by the enzymes acyl‐acyl carrier protein (ACP) thioesterase and β‐keto acyl ACP synthase II. The chain termination reactions of C16:0 and C18:1 are independent, thus paving the way for the possibility of reducing palmitate levels by switching off the palmitoyl ACP thioesterase gene.

Stratum corneum lipids: the effect of ageing and the seasons

Stratum corneum lipids play a predominant role in maintaining the water barrier of the skin. In order to understand the biological variation in the levels and composition of ceramides, ceramide 1 subtypes, cholesterol and fatty acids, stratum corneum lipids collected from tape strippings from three body sites (face, hand, leg) of female Caucasians of different age groups were analysed. In addition, we studied the influence of seasonal variation on the lipid composition of stratum corneum from the same body sites. The main lipid species were quantified using high-performance thin-layer chromatography and individual fatty acids using gas chromatography. Our findings demonstrated significantly decreased levels of all major lipid species, in particular ceramides, with increasing age. Similarly, the stratum corneum lipid levels of all the body sites examined were dramatically depleted in winter compared with spring and summer. The relative levels of ceramide 1 linoleate were also depleted in winter and in aged skin whereas ceramide 1 oleate levels increased. The other fatty acid levels remained fairly constant with both season and age, apart from lignoceric and heptadecanoic acid which showed a decrease in winter compared with summer. The decrease in the mass levels of intercellular lipids and the altered ratios of fatty acids esterified to ceramide 1, are likely to contribute to the increased susceptibility of aged skin to perturbation of barrier function and xerosis, particularly during the winter months.

Studies on red palm oil: Effect of partial supplementation of saturated fats upon lipids and lipoproteins

The effect of partial supplementation of red palm oil (RPO) in saturated fats based on coconut oil (CNO) and hydrogenated fat (HF) was evaluated in a 16-week long experiment in rats. Male rats (wistar strain) were divided into 6 groups and fed with diets based on RPO. Group I with 20% RPO Group II with 20% CNO, group III with 20 HF group IV with 10% RPO and 10% CNO, group V with 10% RPO and 10% HF, and group VI 6.6% RPO and 6.6% CNO and 6.6% HF. The growth of the animals was proportional to the intake of fat and diet. No significant increase was observed in plasma total cholesterol. LDL-C was higher in groups fed with CNO and HF, and HDL-C was higher in the 20% RPO group. The 20% CNO groups had the lowest amount of liver cholesterol when compared to 20% RPO group while the blended oil groups had a higher liver cholesterol. Plasma triglycerides were high in the 20% RPO group whereas in the liver no significant difference observed. Analysis of plasma and liver fatty acids indicated the type of fat consumed as evidenced by the higher levels of palmitate (16:0), oleate (18:1) and linoleate (18:2 n6) in the RPO groups and higher levels of lauric (12:0) myristic (14:0) oleic (18:1) and palmitic (16:0) in 20% CNO groups. The hydrogenated fat group (HF) had a higher levels of lauric (12:0) oleic (18:1) and linoleic acids. The saturated fatty acids (SAFA) supplemented groups in general showed a mixed trend based on the fats. The saturated fatty acids (SAFA) was highest in group II (20% CNO) and group VI (mixed group based on RPO) (CNO and HF) indicating the type of fatty acid intake. PUFA was lowest in CNO group followed by group IV based on RPO and CNO. The various other ratios such as 18:1 18:2 , palmitic oleic ( 16:0 18:1 ) and arachidonic/linoleic ( 20:4 18:2 ) were all normal indicating the type of fat consumed. Thus our present study indicate that supplementation of palm oil (RPO) with other saturated fats like coconut oil and hydrogenated fat (HF) can have a protective effect due to the presence of lipid lowering factors.

Fatty Acid Genotypes of Five Virginia‐Type Peanut Cultivars

Reduction of linoleic acid in the fatty acid profile of Virginia‐type peanut (Arachis hypogaea L.) cultivars is desirable because it would improve the stability and shelf‐life of in‐shell and other peanut products. A low‐linoleate/high‐oleate trait controlled by two recessive genes, ol1 and ol2, has been identified in Univ. of Florida breeding line F435. Most runner‐type cultivars and breeding lines genotyped to date were found to differ from F435 by only one ol allele. Genotypes differing from F435 at two ol loci were Virginia types. The number of genes controlling inheritance of the trait has major implications with respect to the numbers of backcross and F2 test progeny required in an efficient backcross breeding program. To determine the number of genes differentiating F435 from large‐seeded Virginia‐type cultivars, F435 was crossed as a male with five common Virginia‐type cultivars. F4:5 progenies were assayed for fatty acid content by gas chromatography. Progenies were classified as having high or low oleate levels and chi square analysis was applied to the data. Segregation ratios of populations derived from crosses with ‘NC 7’, ‘NC 9’, ‘NC 10C’, and ‘VA‐C 92R’ were consistent with a monogenic model and inconsistent with the digenic model. These cultivars have genotype Ol1Ol1ol2ol2 or ol1ol1Ol2Ol2. Progeny of ‘NC‐V 11’ / F435 followed a ratio consistent with the digenic model and inconsistent with the monogenic model, indicating that NC‐V 11 has genotype Ol1Ol1Ol2Ol2. Oleate levels were elevated by 220 to 280 g kg−1, linoleate levels decreased by 190 to 270 g kg−1, and palmitate levels decreased by 30 to 40 g kg−1 in high‐oleate subpopulations. Other fatty acids exhibited changes that were statistically significant but probably too small in magnitude to significantly alter processing quality or stability of oil.

High-Oleate Oilseeds Fail to Develop at Low Temperature.

The fad2 mutants of Arabidopsis thaliana are deficient in activity of the endoplasmic reticulum oleate desaturase that is the main enzyme responsible for polyunsaturated lipid synthesis in developing seeds of oil crops. A comparison of wild-type and fad2 seeds developing on heterozygous (FAD2/-) plants was used as a model for genetically engineered high-oleate oilseeds of species such as soybean and canola. When fad2 seeds developed at normal temperatures (22[deg]C), they showed high viability compared to wild-type seeds. When a portion of seed development took place at 6[deg]C, germination of the wild-type siblings remained high but germination of fad2 segregants declined considerably. This was true even when exposure to low temperature was limited to the final stages of seed filling and maturation. Compared to wild-type seeds, fully viable fad2 seeds produced at 22[deg]C had reduced lipid contents and were slower to germinate at 10 and 6[deg]C. Taken together, these results indicate that for some oilseed species at least, molecular genetic manipulation of oleate levels in the oil may result in plant lines with unacceptable performance in the field.