Up-Regulation of Stearoyl-CoA Desaturase 1 Increases Liver MUFA Content in Obese Zucker but Not Goto-Kakizaki Rats

The Goto-Kakizaki (GK) rat is an animal model for spontaneous-onset, non-obese type 2 diabetes. Despite abundant evidence about disorders in metabolism, little information is available about fatty acid metabolism in the liver of GK rats. This study aimed to investigate the characteristics of the fatty acid profile, particularly MUFA, and the mechanism underlying the alterations in fatty acid profiles in the liver of GK rats. The activities of enzymes that participate in the biosynthesis of MUFA, expressions of genes encoding these enzymes, and the fatty acid profile in the liver were compared with those of obese Zucker (fa/fa) (ZF) rats, which are obese and non-diabetic. Stearoyl-CoA desaturase (SCD) activity and SCD1 gene expression were considerably up-regulated in GK rats, and these levels were largely comparable to those in ZF rats. However, the proportions and contents of oleic acid and palmitoleic acid were very low considering the highly elevated activity of SCD in the liver of GK rats, when compared with ZF rats. Palmitoyl-CoA chain elongation (PCE) activity and fatty acid elongase (Elovl6) gene expression were markedly up-regulated in ZF rats, whereas PCE activity was up-regulated much less and Elovl6 gene expression was unchanged in GK rats. These results suggest the possibility that up-regulation of gene expression of Elovl6 along with SCD1 is indispensable to elevate the proportions and contents of oleic acid in the liver.     

Fatty Acid de Novo Synthesis in Adult Intrauterine Growth-Restricted Offspring,and Adult Male Response to a High Fat Diet

Intrauterine growth restriction (IUGR) with rapid catch‐up growth leads to adult obesity and insulin resistance. We have previously shown that IUGR male rats demonstrated increased de novo fatty acid synthesis in the subcutaneous (SC) fat, but not the visceral fat, during the nursing period prior to the onset of obesity. Young IUGR females do not exhibit the same increase. We further hypothesized that in male IUGR offspring, de novo synthesis is a programmed intrinsic effect that persists to adulthood and does not suppress in response to a high fat diet. We measured fatty acid de novo synthesis in IUGR adult males (6 months) using deuterium‐enriched drinking water as a stable isotope tracer, then further studied the response after consumption of an isocaloric high fat diet. Baseline de novo synthesis in adult females was also studied at age 9 months. Males demonstrated increased baseline de novo synthesis in both SC fat and visceral fat. Correspondingly, SC and visceral fat protein expression of lipogenic enzymes acetyl‐coA carboxylase‐α (ACCα) and fatty acid synthase were upregulated. After the isocaloric high fat diet, de novo synthesis was suppressed such that no differences remained between the two groups, although, IUGR SC fat demonstrated persistently increased lipogenic protein expression. In contrast, de novo synthesis among adult females is not impacted in IUGR. In conclusion, enhancement of male IUGR SC fat de novo synthesis appears to be an early consequence of metabolic programming, whereas enhancement in visceral fat appears to be a later consequence.     

Conjugated linoleic acid reduces hepatic steatosis, improves liver function, and favorably modifies lipid metabolism in obese insulin-resistant rats

CLA has been shown to induce or suppress excess liver lipid accumulation in various animal models. Interestingly, the state of insulin resistance may be an important modulator of this effect. The objective of the current study was to determine how feeding a dietary CLA mixture would affect liver lipid accumulation in insulin-resistant/obese and lean rats in relation to liver function, lipidemia, liver TAG and phospholipid FA composition, and expression of hepatic markers of FA transport, oxidation, and synthesis. Six-week-old fa/fa and lean Zucker rats (n=20/genotype) were fed either a 1.5% CLA mixture or a control diet for 8 wk. CLA supplementation reduced liver lipid concentration of fa/fa rats by 62% in concurrence with improved liver function (lower serum alanine aminotransferase and alkaline phosphatase) and favorable modification of the serum lipoprotein profile (reduced VLDL and LDL and elevated HDL) compared with control-fed fa/fa rats. The fa/fa genotype had two-thirds the amount of CLA (as % total FA) incorporated into liver TAG and phospholipids compared with the lean genotype. In both genotypes, CLA altered the hepatic FA profile (TAG greater than phospholipids) and these changes were explained by a desaturase enzyme index. Liver-FA-binding protein and acyl CoA oxidase, markers of FA transport and oxidation, respectively, were expressed at higher levels in CLA-fed fa/fa rats. In summary, these results illustrate a strong relationship between the state of insulin resistance and liver lipid metabolism and suggest that CLA acts to favorably modify lipid metabolism in fa/fa Zucker rats.     

Reduced Maternal Erythrocyte Long Chain Polyunsaturated Fatty Acids Exist in Early Pregnancy in Preeclampsia

The present prospective study examines proportions of maternal erythrocyte fatty acids across gestation and their association with cord erythrocyte fatty acids in normotensive control (NC) and preeclamptic pregnancies. We hypothesize that maternal fatty acid status in early pregnancy influences fetal fatty acid stores in preeclampsia. 137 NC women and 58 women with preeclampsia were included in this study. Maternal blood was collected at 3 time points during pregnancy (16–20th weeks, 26–30th weeks and at delivery). Cord blood was collected at delivery. Fatty acids were analyzed using gas chromatography. The proportions of maternal erythrocyte α‐linolenic acid, docosahexaenoic acid, nervonic acid, and monounsaturated fatty acids (MUFA) (p < 0.05 for all) were lower while total n‐6 fatty acids were higher (p < 0.05) at 16–20th weeks of gestation in preeclampsia as compared with NC. Cord 18:3n‐3, 22:6n‐3, 24:1n‐9, MUFA, and total n‐3 fatty acids (p < 0.05 for all) were also lower in preeclampsia as compared with NC. A positive association was observed between maternal erythrocyte 22:6n‐3 and 24:1n‐9 at 16–20th weeks with the same fatty acids in cord erythrocytes (p < 0.05 for both) in preeclampsia. Our study for the first time indicates alteration in maternal erythrocyte fatty acids at 16th weeks of gestation which is further reflected in cord erythrocytes at delivery in preeclampsia.     

Effects of lovastatin on hepatic fatty acid metabolism

Thein vitro andin vivo effects of lovastatin on fatty acid metabolism were studied in isolated rat hepatocytes. When addedin vitro to cell incubations, lovastatin stimulatedde novo fatty acid synthesis and acetyl-CoA carboxylase activity, whereas fatty acid synthase, activity was unaffected. Lovastatin depressed palmitate, but not octanoate, oxidation. This may be attributed to the lovastatin-induced increase, in intracellular malonyl-CoA levels, as no concomitant changes of carnitine palmitoyltransferase I (CPT-I) specific activity was detected. Lovastatin had no effect on the synthesis and secretion of triacylglycerols and phospholipids in the form of very low density lipoproteins (VLDL). When rats were fed a diet supplemented with 0.1% (w/w) lovastatin for one week, both acetyl-CoA carboxylase activity andde novo fatty acid synthesis were reduced compared to pair-fed controls, whereas fatty acid synthase activity was unaffected. Palmitate oxidation was enhanced in the lovastatin-fed group. There was an increase in CPT-I activity but no change in intracellular concentration of malonyl-CoA. Lovastatin feeding and no significant effect either on the esterification of exogenous palmitic acid into both cellular and VLDL triacylglycerols and phospholipids or on hepatic lipid accumulation. Thein vitro andin vivo effects of lovastatin were not significantly different between periportal and perivenous hepatocytes. The results indicate that: (i) the administration of lovastatin increased the fatty acid-oxidative capacity of the liver at the expense of its lipogenic capacity, (ii) the rate ofde novo cholesterol synthesis did not seem to be a limiting factor in the synthesis and secretion of VLDL and (iii) lovastatin produced opposite effects on hepatic fatty acid metabolismin vitro andin vivo.     

High-Fat Diet Alters Serum Fatty Acid Profiles in Obesity Prone Rats: Implications for In Vitro Studies

High‐fat diets (HFD) are commonly used in rodents to induce obesity, increase serum fatty acids and induce lipotoxicity in various organs. Invitro studies commonly utilize individual free fatty acids (FFA) to study lipid exposure in an effort to model what is occurring in vivo; however, these approaches are not physiological as tissues are exposed to multiple fatty acids in vivo. Here we characterize circulating lipids in obesity‐prone rats fed an HFD in both fasted and fed states with the goal of developing physiologically relevant fatty acid mixtures for subsequent in vitro studies. Rats were fed an HFD (60 % kcal fat) or a control diet (10 % kcal fat) for 3 weeks; liver tissue and both portal and systemic blood were collected. Fatty acid profiles and absolute concentrations of triglycerides (TAG) and FFA in the serum and TAG, diacylglycerol (DAG) and phospholipids in the liver were measured. Surprisingly, both systemic and portal serum TAG were ~40 % lower in HFD‐fed compared to controls. Overall, compared to the control diet, HFD feeding consistently induced an increase in the proportion of circulating polyunsaturated fatty acids (PUFA) with a concomitant decline in monounsaturated fatty acids (MUFA) and saturated fatty acids (SFA) in both serum TAG and FFA. The elevations of PUFA were mostly attributed to increases in n‐6 PUFA, linoleic acid and arachidonic acid. In conclusion, fatty acid mixtures enriched with linoleic and arachidonic acid in addition to SFA and MUFA should be utilized for in vitro studies attempting to model lipid exposures that occur during in vivo HFD conditions.     

Oxidation of intracellular and extracellular fatty acids in skeletal muscle

Fatty acids are a major fuel for many tissues, and abnormal utilization is implicated in diseases. However, tissue fatty acid oxidation has not been determined reliably in vivo. Furthermore, fatty acid oxidation has not been partitioned into intracellular and extracellular components. In this report, a one‐pool model is described that enables direct quantitation of fluxes of intracellular and plasma fatty acids to mitochondria in skeletal muscle using dual stable isotopes and liquid chromatography/electrospray ionization ion‐trap tandem mass spectrometry technology. It is validated by the determination of palmitate oxidation by skeletal muscle in lean and obese rats and the regulation by insulin. Resting postabsorptive intramyocellular and plasma palmitate oxidation by the gastrocnemius muscle was determined to be 3.47 ± 0.8 and 2.06 ± 0.5 nmol/g/min in lean and 6.96 ± 1.8 and 1.34 ± 0.2 nmol/g/min in obese rats, respectively. In obese rats, hyperinsulinemia (1 nmol/L) suppressed intramyocellular (by 59 ± 5% to 2.88 ± 0.3 nmol/g/min; p <0.05) but not plasma (1.41 ± 0.14 nmol/g/min; p >0.05) palmitate oxidation. The fractional turnover rate of palmitoylcarnitine (0.34 ± 0.1/min vs. 0.83 ± 0.2/min; p <0.05) was also suppressed by insulin in obese rats. In obese and lean rats, 83 and 51%, respectively (p = 0.08), of plasma fatty acids traverse the triacylglycerol pool before being oxidized. The results demonstrated that the methodology is feasible and sensitive to metabolic alterations and thus can be used to study fatty acid utilization at tissue level in vivo in a compartmentalized manner for the first time.     

Hypolipidemic Effects of Phospholipids (PL) Containing n-3 Polyunsaturated Fatty Acids (PUFA) Are Not Dependent on Esterification of n-3 PUFA to PL

Phospholipids (PL) containing n‐3 polyunsaturated fatty acids (PUFA) have beneficial effects of maintaining and promoting health compared with triacylglycerols (TAG) containing n‐3 PUFA or general PL. This study evaluated the effects of dietary PL containing n‐3 PUFA and elucidated the effects of the glycerophosphate structure and n‐3 PUFA on fatty acid (FA) metabolism in rats. Rats were fed a basal diet containing soybean oil alone, TAG containing n‐3 PUFA (1.8 %), soybean PL (2.7 %), PL containing n‐3 PUFA (2.7 %), or TAG containing n‐3 PUFA (1.8 %) + soybean PL (2.7 %). The present n‐3 PUFA‐supplemented diets had similar FA compositions, and the PL diets had similar PL compositions. TAG containing n‐3 PUFA reduced serum TAG contents, but did not affect serum cholesterol contents compared with soybean oil alone. PL diets containing n‐3 PUFA and the combination of TAG containing n‐3 PUFA and soybean PL resulted in decreased serum and liver TAG contents compared with the diet containing soybean oil alone, reflecting enhanced liver FA β‐oxidation. The results of this study show that TAG containing n‐3 PUFA with added soybean PL affects serum and liver TAG and cholesterol contents to a similar degree as PL containing n‐3 PUFA. TAG containing n‐3 PUFA and soybean PL are widely used as functional food ingredients and pharmaceutical constituents and are inexpensive compared with PL containing n‐3 PUFA. Therefore, the combination of TAG containing n‐3 PUFA and soybean PL has potential as a useful and inexpensive component of functional foods.     

Lipid composition of hepatocyte plasma membranes from geese overfed with corn

Twelve-week-old Landes male geese were overfed with corn for 21 d in order to induce liver steatosis (fatty liver). Lipid composition of hepatocyte plasma membranes from fatty livers was compared to that of lean livers obtained from geese fed a normal diet. The ratio cholesterol/phospholipids was higher in fatty hepatocyte plasma membranes (0.63 vs. 0.47), whereas the phospholipid/protein ratio was less than half. Overfeeding induced changes in fatty acid composition of hepatocyte plasma membranes, including a greater than twofold increase in the percentage of oleic acid (29.7 vs. 13.8%) and a somewhat lesser increase in lauric, palmitic, and palmitoleic acid contents of plasma membrane lipids of fatty livers. A concomitant reduction in the proportion of stearic acid (18.4 vs. 25.1%) was also observed. In fatty livers, the increased ratio of saturated to polyunsaturated fatty acids (PUFA) (1.5 vs. 1.0) was related to a significant decrease in PUFA content. Among all the PUFA, only the eicosatrienoic acid (20∶3n−9) percentage was increased by liver steatosis. Overfeeding with corn appeared to induce competition between de novo synthesized and dietary fatty acids incorporated in hepatocyte plasma membranes. This resulted in an accumulation of de novo synthesized monounsaturated and derived fatty acids in plasma membranes from overfed birds. A defect in the incorporation of linoleic acid and linoleic- and linolenic-derived PUFA was observed despite the high proportion of these essential fatty acids in the diet. It was conclued that in overfed palmipeds, de novo hepatic lipogenesis prevails over dietary lipid intake to modulate lipid composition of the fatty liver plasma membrane.     

Effects of perfluorodecanoic acid onde novo fatty acid and cholesterol synthesis in the rat

Perfluorodecanoic acid (PFDA) is a peroxisome proliferator that causes a dose-dependent (20–80 mg/kg) increase in hepatic triacylglycerol and cholesteryl ester levels in the rat. We hypothesized that PFDA may cause an increase in thede novo synthesis of fatty acids and cholesterol in this species, which would explain observed effects. The incorporation of³H₂O into tissue lipids was examined 7 days after rats received vehicle or 20 or 80 mg/kg of PFDA. PFDA treatment decreased the rate of synthesis of cholesterol and fatty acids in the liver and in epididymal fat pad. At a PFDA dose (20 mg/kg) that decreasedde novo synthesis of fatty acids and cholesterol, there was no effect on the concentration of fatty acids and cholesterol in the liver, epididymal fat pads, and plasma. We conclude that PFDA induced fatty liver is due to either a decrease in the oxidation of fatty acids in the liver, or an impairment of triacylglycerol catabolism and/or export from the liver, and is not the result of an increase inde novo synthesis of fatty acids and cholesterol.     

Regiospecific distribution of fatty acids in triacylglycerols and phospholipids from broad beans (Vicia faba)

Regiospecific distributions of fatty acids of triacylglycerols (TAG) and phospholipids (PL) separated from broad beans (Vicia faba) of four cultivars (Minpo, Sanuki, Nintoku and Sanren) were investigated. The major lipid components were PL (47.5–50.5 wt‐%) and TAG (47.7–50.1 wt‐%), while steryl esters, hydrocarbons, free fatty acids, diacylglycerols and monoacylglycerols were present in minor proportions (1.6–2.4 wt‐%). The PL components isolated from the four cultivars were phosphatidylcholine (56.4–58.4 wt‐%), phosphatidylethanolamine (20.3–21.7 wt‐%) and phosphatidylinositol (16.6–18.6 wt‐%). Phosphatidylinositol was unique in that it had the highest saturated fatty acid content among these PL. The principal characteristics of the fatty acid distribution in the TAG and PL were evident in the beans: Unsaturated fatty acids were predominantly concentrated in the sn‐2 position while saturated fatty acids primarily occupied the sn‐1 or sn‐3 position in these lipids. The lipid components and fatty acid distributions were almost the same in the four cultivars and were not influenced by genetic variability and planting location. These results could be useful information to both consumers and producers for the manufacture of traditional broad bean foods in Japan.     

Influence of native antioxidants on the formation of fatty acid hydroperoxides in model systems

The effect of alpha‐tocopherol (alpha‐T) and quercetin on the formation of hydroperoxides of linoleic and linolenic acids during autoxidation at 60 ± 1 °C was investigated. Three isomers of hydroperoxides were detected using HPLC. Of isomers of linoleic acid hydroperoxides, 13‐hydroperoxy‐octadecadienoic acid trans‐trans (13‐HPODE t‐t), 9‐HPODE cis‐trans (9‐HPODE c‐t) and 9‐HPODE trans‐trans (9‐HPODE t‐t) were identified, constituting 64, 19 and 17% of the total amount, respectively. For linolenic acid, the components 13‐hydroperoxy‐octadecatrienoic acid trans‐trans (13‐HPOTE t‐t), 9‐HPOTE c‐t and 9‐HPOTE t‐t contributed 7, 33 and 60% to the total, respectively. The different dominant hydroperoxide isomers detected in linoleic and linolenic acids during oxidation are related to their chemical structure and the microenvironment of emulsion droplets. The ratios between specific isomers for both fatty acid hydroperoxides did not change during oxidation with or without antioxidants. Alpha‐T effectively inhibited the oxidation of fatty acids and reduced the formation of hydroperoxides. The total amount of the hydroperoxides decreased along with the increase in the concentration of alpha‐T, 1–40 µM. Quercetin inhibited the oxidation of both fatty acids at similar efficiency only at 40 µM concentration. A synergistic antioxidant effect of quercetin with alpha‐T in a binary system on both fatty acids was observed.     

Fatty acid profiles in tissues of mice fed conjugated linoleic acid

The incorporation of vaccenic acid (VA, 0.5 and 1.2%), conjugated linoleic acid (CLA, mixture of primarily c9,t11‐ and t10,c12‐CLA, 1.2%), linoleic acid (LA, 1.2%) and oleic acid (OA, 1.2%) into different tissues of mice was examined. The effects on the fatty acid composition of triacylglycerols (TAG) and phospholipids (PL) in kidney, spleen, liver and adipose tissue were investigated. VA and CLA (c9,t11‐ and t10,c12‐CLA) were primarily found in TAG, especially in kidney and adipose tissue, respectively. Conversion of VA to c9,t11‐CLA was indicated by our results, as both fatty acids were incorporated into all the analyzed tissues when a diet containing VA but not c9,t11‐CLA was fed. Most of the observed effects on the fatty acid profiles were seen in the CLA group, whereas only minor effects were observed in the VA groups compared with the OA group. Thus, CLA increased n‐3 polyunsaturated fatty acids (PUFA) in PL from kidney and spleen and lowered the ratio of n‐6/n‐3 PUFA in these tissues. Furthermore, CLA increased C₂₂ PUFA in the PL fraction of kidney, spleen and liver, but reduced the level of arachidonic acid in PL of liver and spleen and lowered the Δ⁹‐desaturation indexes in all analyzed tissue TAG.     

Positional distribution of fatty acids in triacylglycerols and phospholipids from adzuki beans (Vigna angularis)

The fatty acid distributions of triacylglycerols (TAG) and major phospholipids (PL) obtained from adzuki beans (Vigna angularis) were investigated. The total lipids extracted from the beans were separated by thin‐layer chromatography (TLC) into eight fractions. The major lipid components were PL (63.5 wt‐%), TAG (21.2 wt‐%), steryl esters (7.5 wt‐%) and hydrocarbons (5.1 wt‐%), while free fatty acids, diacylglycerols (1,3‐DAG and 1,2‐DAG) and monoacylglycerols were also present in minor proportions (0.2–1.1 wt‐%). The major PL components isolated from the beans were phosphatidylcholine (45.3 wt‐%), phosphatidylethanolamine (25.8 wt‐%) and phosphatidylinositol (21.5 wt‐%). Phosphatidylinositol was unique in that it had the highest saturated fatty acid content among the three PL. With a few exceptions, however, the principal characteristics of the fatty acid distribution in the TAG and three PL were evident in the beans: Unsaturated fatty acids were predominantly concentrated in the sn‐2 position while saturated fatty acids primary occupied the sn‐1 or sn‐3 position in the oils of the adzuki beans. In general, these results could be useful to both consumers and producers for the manufacture of traditional adzuki foods in Japan.     

Characterization of the glycerolipid composition of a high‐palmitoleic acid sunflower mutant

The glycerolipid composition of a high‐palmitoleic acid sunflower (Helianthus annuus L.) mutant accumulating up to 20% of n‐7 fatty acids was studied. This line produces oil with a complex triacylglycerol (TAG) composition, containing species that have not been previously identified in sunflower. In this regard, palmitoleic acid was esterified in an unexpected way in the three positions of the TAG molecules. The polar glycerolipid composition of the mutant was also studied, in order to identify and quantify the changes in membrane lipids imposed by the sunflower enzymatic machinery during the accumulation of the unusual n‐7 fatty acids. The high‐palmitoleic mutant accumulated important quantities of n‐7 fatty acids in the polar lipid fraction, especially in the phosphatidylcholine lipid class. However, the total polar lipid content of these lines was not affected. On the other hand, the mutations responsible for the n‐7 lipid accumulation induced an important decrease in the oil yield of the new mutant.     

Maternal High‐Fat‐Diet Programs Rat Offspring Liver Fatty Acid Metabolism

In offspring exposed in utero to a maternal diet high in fat (HF), we have previously demonstrated that despite similar birth weights, HF adult offspring at 6 months of age had significantly higher body weights, greater adiposity, and increased triacylglycerol (TAG) levels as compared to controls. We hypothesized that a maternal HF diet predisposes to offspring adiposity via a programmed increase in the synthesis of monounsaturated fatty acids in the liver and hence increased substrate availability for liver TAG synthesis. We further hypothesized that programmed changes in offspring liver fatty acid metabolism are associated with increased liver expression of the lipogenic enzyme stearoyl‐CoA desaturase‐1 (SCD‐1). Female rats were maintained on a HF diet rich in monounsaturated fatty acids (MUFA) prior to and throughout pregnancy and lactation. After birth, newborns were nursed by the same dam, and all offspring were weaned to control diet. Plasma and liver fatty acid compositions were determined using gas chromatography/mass spectrometry. Fatty acid C16 desaturation indices of palmitoleic/palmitic and (vaccenic + palmitoleic)/palmitic and the C18 desaturation index of oleic/stearic were calculated. Liver protein abundance of SCD‐1 was analyzed in newborns and adult offspring. Plasma and liver C16 desaturation indices were decreased in HF newborns, but increased in the adult offspring. Liver SCD‐1 expression was increased in the HF adult offspring. These data show that the maternal HF diet during pregnancy and lactation increases offspring liver SCD‐1 protein abundance and alters the liver C16 desaturase pathway.     

Sex‐specific Alterations in Serology and the Expression of Liver FATP4 Protein in Offspring Exposed to High‐Fat Diet during Pregnancy and/or Lactation

Changes in dietary composition will have a significant impact on the nutritional status of the mother and the offspring. To examine the relevant hormone level changes during lactation and the expression of fatty acid transporters in the placenta and liver under the condition of a high‐fat (HF) diet, we established HF animal models and conducted a cross‐fostering program to mimic the shift in diet. On gestation day (GD)18, the weight of placenta in the HF group was significantly higher than that in the control group (p < 0.05). HF‐fed male pups had a significantly lower serum insulin level, but the same phenomenon was not found in females. On the contrary, serum triacylglycerol (TAG) level presented a tendency to decrease only in female offspring. Oil red O staining showed lipid accumulation in the HF diet offspring livers. The mRNA levels of FATP4 in the placenta in the HF diet group were significantly upregulated compared to the control diet group (p < 0.05). High‐fat diet (HFD) consumption also altered the liver mRNA levels of FATP4, SREBP‐1, and SCD‐1 in the male offspring, while the changes in protein levels of FATP4 were not observed in either sex. In conclusion, maternal HF diet has a profound impact on offspring growth, metabolism, and the risk of metabolic disorders, which would depend on the exposure period of pregnancy and lactation.     

Regional distribution in the fatty acids of triacylglycerols and phospholipids within soybean seeds (Glycine max L.)

The fatty acid distribution of triacylglycerols (TAG) and major phospholipids (PL) within soybean seeds (Glycine max L.) was investigated in relation to their tocopherol contents. The lipids extracted from four cultivars were separated by thin‐layer chromatography into seven fractions. Tocopherols were predominantly detected in the axis, followed by cotyledons and seed coat. The major lipid components were TAG and PL, while hydrocarbons, steryl esters, free fatty acids and diacylglycerols (sn‐1,3 and sn‐1,2) were also present in minor proportions. With a few exceptions, the dominant PL components were phosphatidylcholine, followed by phosphatidylethanolamine or phosphatidylinositiol. Significant differences (p <0.05) in fatty acid distribution existed when different soybean cultivars were examined. However, the principal characteristics of the fatty acid distribution in the TAG were evident among four cultivars; unsaturated fatty acids were predominantly concentrated in the sn‐2 position, and saturated fatty acids primarily occupied the sn‐1 or sn‐3 position in the oils of the soybeans.     

Response of plasma lipids to dietary cholesterol and wine polyphenols in rats fed polyunsaturated fat diets

This experiment was designed to evaluate the effects of dietary red wine phenolic compounds (WP) and cholesterol on lipid oxidation and transport in rats. For 5 wk, weanling rats were fed polyunsaturated fat diets (n−6/n−3=6.4) supplemented or not supplemented with either 3 g/kg diet of cholesterol, 5 g/kg diet of WP, or both. The concentrations of triacylglycerols (TAG, P<0.01) and cholesterol (P<0.0002) were reduced in fasting plasma of rats fed cholesterol despite the cholesterol enrichment of very low density lipoprotein + low density lipoprotein (VLDL+LDL). The response was due to the much lower plasma concentration of high density lipoprotein (HDL) (−35%, P<0.0001). In contrast, TAG and cholesteryl ester (CE) accumulated in liver (+120 and +450%, respectively, P<0.0001). However, the cholesterol content of liver microsomes was not affected. Dietary cholesterol altered the distribution of fatty acids mainly by reducing the ratio of arachidonic acid to linoleic acid (P<0.0001) in plasma VLDL+LDL (−35%) and HDL (−42%) and in liver TAG (−42%), CE (−78%), and phospholipids (−28%). Dietary WP had little or no effect on these variables. On the other hand, dietary cholesterol lowered the α-tocopherol concentration in VLDL+LDL (−40%, P<0.003) and in microsomes (−60%, P<0.0001). In contrast, dietary WP increased the concentration in microsomes (+21%, P<0.0001), but had no effect on the concentration in VLDL+LDL. Cholesterol feeding decreased (P<0.006) whereas WP feeding increased (P<0.0001) the resistance of VLDL+LDL to copper-induced oxidation. The production of conjugated dienes after 25 h of oxidation ranged between 650 (WP without cholesterol) and 2,560 (cholesterol without WP) μmol/g VLDL+LDL protein. These findings show that dietary WP were absorbed at sufficient levels to contribute to the protection of polyunsaturated fatty acids in plasma and membranes. They could also reduce the consumption of α-tocopherol and endogenous antioxidants. The responses suggest that, in humans, these substances may be beneficial by reducing the deleterious effects of a dietary overload of cholesterol.