Dietary Supplementation of Lauric Acid Alleviates the Irregular Estrous Cycle and the Impaired Metabolism and Thermogenesis in Female Mice Fed with High-Fat Diet (HFD).

Lauric acid (LA) has been implicated in the prevention/treatment of obesity. However, the role of LA in modulating an obesity-related female reproductive disorder remains largely unknown. Here, female mice were fed a control diet, high-fat diet (HFD), or HFD supplemented with 1% LA. The results demonstrated that the HFD-induced estrous cycle irregularity and the reduction of serum follicle-stimulating hormone (FSH) were alleviated by LA supplementation. In possible mechanisms, LA supplementation led to significant increase in serum lipid metabolites such as sphingomyelin and lysophosphatidylcholine containing LA (C12:0) and the improvement of glucose metabolism in mice fed HFD. Moreover, impaired body energy metabolism and weakened brown adipose tissue (BAT) thermogenesis of HFD-fed mice were improved by LA supplementation. Together, these findings showed that LA supplementation alleviated HFD-induced estrous cycle irregularity, possibly associated with altered serum lipid metabolites, improved glucose metabolism, body energy metabolism, and BAT thermogenesis. These findings suggested the potential application of LA in alleviating obesity and its related reproductive disorders.

In situ fabrication of mesoporous silica-coated silver-gold hollow nanoshell for remotely controllable chemo-photothermal therapy via phase-change molecule as gatekeepers.

This study reports a new strategy for in situ fabrication of plasmonic hollow silver-gold nanoshell (with resonance tuned to NIR region) encased in the hollow mesoporous silica as an efficient platform to efficiently and precisely regulate the release of 5-fluorouracil (anticancer drug) for prostate cancer therapy and photothermal therapy. The mesopores were capped with thermosensitive phase-change material lauric acid, which allowed for remote, precise, and spatiotemporal control of drug release via external heating or photothermal heating of plasmonic silver-gold nanoshell via NIR laser irradiation. The system was nanometric, monodispersed, and showed negative surface charge. The nanocarrier showed better pH stability and thermodynamic stability compared to dense silica-coated gold nanoshells. The drug release could be triggered remotely by applying low powered continuous wave NIR laser (λ = 808 nm). The nanocarrier showed improved internalization by cancer cells, which was further enhanced by laser irradiation. High powered laser directly killed the cancer cells via photothermal effect in the region irradiated. Thus, this system fabricated by novel synthetic strategy provided efficient chemo- and phototherapy.

Effects of feeding lauric acid or coconut oil on ruminal protozoa numbers, fermentation pattern, digestion, omasal nutrient flow, and milk production in dairy cows.

The objectives of this study were to evaluate the feeding of coconut oil (CO), in which lauric acid (La) comprises about 50% of the fatty acid composition, as a practical rumen protozoa (RP) suppressing agent, to assess whether the source of La affects ruminal fermentation and animal performance and to test whether suppressing RP improves N utilization, nutrient digestion, nutrient flow at the omasal canal, and milk production. Fifteen multiparous Holstein cows (3 fitted with ruminal cannulas) and 15 primiparous Holstein cows (3 fitted with ruminal cannulas) were used in a replicated 3×3 Latin square experiment with 14d of adaptation and 14d of sample collection. Diets were fed as total mixed ration and contained (dry matter basis) 10% corn silage, 50% alfalfa silage, and 40% concentrate. The control diet contained 3% (dry matter basis) calcium soaps of palm oil fatty acids (Megalac, Church & Dwight Co. Inc., Princeton, NJ) as a ruminally inert fat source and had no added La or CO. Diets with La and CO were formulated to contain equal amounts of La (1.3%, dry matter basis). Dry matter intake was not affected by treatment. Both CO and La reduced RP numbers by about 40%. Lauric acid reduced yield of milk and milk components; however, CO did not affect yield of milk and yields of milk components. Both La and CO caused small reductions in total VFA concentration; CO increased molar proportion of ruminal propionate, reduced ruminal ammonia and branched-chain volatile fatty acids, suggesting reduced protein degradation, and reduced milk urea N and blood urea N concentrations, suggesting improved protein efficiency. Lauric acid reduced total-tract apparent digestibility of neutral detergent fiber and acid detergent fiber as well as ruminal apparent digestibility of neutral detergent fiber and acid detergent fiber as measured at the omasal canal; however, CO did not alter fiber digestion. Microbial protein flow at the omasal canal, as well as the flow of N fractions at the omasal canal, did not differ among treatments. Results from this experiment have confirmed that dietary La is not a practical agent for suppressing RP population in dairy cows, mainly because of its negative effects on fiber digestion and ruminal fermentation. Intake of CO appeared to reduce ruminal and improve protein efficiency, but did not improve milk production, milk composition, or increase microbial outflow from the rumen. Based on the results of this study, a 40% reduction of RP population is not sufficient to improve N utilization in dairy cows.

Saturated fatty acids intake in relation to C-reactive protein, adiponectin, and leptin: a population-based study.

OBJECTIVE: Evidence on the relation of saturated fatty acids (SFA) with inflammatory markers and adipokines is scarce and inconsistent. This study aimed to evaluate the association of the intake of total SFA, their subtypes (lauric, myristic, palmitic, and stearic acids), and SFA to polyunsaturated fatty acids (PUFA) ratio (SFA/PUFA ratio) with serum concentrations of high-sensitivity C-reactive protein (hs-CRP), adiponectin, and leptin among Portuguese adults. METHODS: We studied 395 non-institutionalized inhabitants of Porto (52.2% women; age range: 26-64 y) who were evaluated in 2010-2011, as part of EPIPorto study. Fatty acids intake was assessed with a validated semi-quantitative food frequency questionnaire. Blood was sampled after an overnight fast and serum concentrations of hs-CRP (through particle-enhanced immunonephelometry), adiponectin, and leptin (through radioimmunoassay) were determined. Regression coefficients (ß) and 95% confidence intervals (CI) were obtained from linear regression models, stratified by sex. RESULTS: After adjusting for age, education, regular physical exercise, smoking, and central body fat percentage, hs-CRP was significantly and positively associated with lauric (ß = 0.218; 95% CI, 0.071-0.365) and myristic acids (ß = 0.220; 95% CI, 0.073-0.368) and with SFA/PUFA ratio (ß = 0.171; 95% CI, 0.022-0.320) in men, but not in women. For adiponectin and leptin, no significant associations with SFA intake were observed in either sex. CONCLUSIONS: A detrimental role of lauric and myristic acids and of high SFA/PUFA ratio is suggested by their association with elevated hs-CRP concentrations in men. Our findings may be helpful in the planning of dietary modifications aimed at the modulation of inflammatory activity that could be an intermediate step to coronary events.

Activity of virgin coconut oil, lauric acid or monolaurin in combination with lactic acid against Staphylococcus aureus.

The objective of this study was to investigate the in vitro activities of virgin coconut oil, lauric acid and monolaurin in combination with lactic acid against two strains of Staphylococcus aureus, ATCC 25923 and an isolate from a pig carcass, by determination of Fractional Bactericidal Concentration Index (FBCI), time-kill method, as well as scanning and transmission electron microscopy. Minimum bactericidal concentrations (MBC) of lauric acid, monolaurin and lactic acid were 3.2 mg/ml, 0.1 mg/ml and 0.4% (v/v), respectively. The effects of lauric acid + lactic acid and monolaurin + lactic acid combinations were synergistic against both strains, exhibiting FBCIs of 0.25 and 0.63, respectively. In time-kill studies, lauric acid and monolaurin + lactic acid combinations added at their minimum inhibitory concentrations produced a bactericidal effect. The induction of stress in non-stressed cells was dependent on the type and concentration of antimicrobial. This resulted in a loss and change of the cytoplasm and membrane in cells of the bacterium. In contrast, virgin coconut oil (10%) was not active against S. aureus. The bacterial counts found in pork loin treated with lauric acid and monolaurin alone were significantly higher (p <0.05) than those treated with both lipids in combination with lactic acid at sub-inhibitory concentrations. The color, odor and overall acceptability of the pork loins were adversely affected by treatment with the three lipids and lactic acid alone but when combinations of the agents were used the sensory quality was acceptable.

Link between lipid metabolism and voluntary food intake in rainbow trout fed coconut oil rich in medium-chain TAG.

We examined the long-term effect of feeding coconut oil (CO; rich in lauric acid, C12) on voluntary food intake and nutrient utilisation in rainbow trout (Oncorhynchus mykiss), with particular attention to the metabolic use (storage or oxidation) of ingested medium-chain TAG. Trout were fed for 15 weeks one of the four isoproteic diets containing fish oil (FO) or CO as fat source (FS), incorporated at 5% (low fat, LF) or 15% (high fat, HF). Fat level or FS did not modify food intake (g/kg(0·8) per d), despite higher intestinal cholecystokinin-T mRNA in trout fed the HF-FO diet. The HF diets relative to the LF ones induced higher growth and adiposity, whereas the replacements of FO by CO resulted in similar growth and adiposity. This, together with the substantial retention of C12 (57% of intake), suggests the relatively low oxidation of ingested C12. The down-regulation of carnitine palmitoyl-transferase-1 (CPT-1) confirms the minor dependency of medium-chain fatty acids (MCFA) on CPT-1 to enter the mitochondria. However, MCFA did not up-regulate mitochondrial oxidation evaluated using hepatic hydroxyacyl-CoA dehydrogenase as a marker, in line with their high retention in body lipids. At a low lipid level, MCFA increased mRNA levels of fatty acid synthase, elongase and stearoyl-CoA desaturase in liver, showing the hepatic activation of fatty acid synthesis pathways by MCFA, reflected by increased 16 : 0, 18 : 0, 16 : 1, 18 : 1 body levels. The high capacity of trout to incorporate and transform C12, rather than to readily oxidise C12, contrasts with data in mammals and may explain the absence of a satiating effect of CO in rainbow trout.

Effects of a combination of feed additives on methane production, diet digestibility, and animal performance in lactating dairy cows.

Two experiments were conducted to assess the effects of a mixture of dietary additives on enteric methane production, rumen fermentation, diet digestibility, energy balance, and animal performance in lactating dairy cows. Identical diets were fed in both experiments. The mixture of feed additives investigated contained lauric acid, myristic acid, linseed oil, and calcium fumarate. These additives were included at 0.4, 1.2, 1.5, and 0.7% of dietary dry matter, respectively (treatment ADD). Experimental fat sources were exchanged for a rumen inert source of fat in the control diet (treatment CON) to maintain isolipidic rations. Cows (experiment 1, n=20; experiment 2, n=12) were fed restricted amounts of feed to avoid confounding effects of dry matter intake on methane production. In experiment 1, methane production and energy balance were studied using open-circuit indirect calorimetry. In experiment 2, 10 rumen-fistulated animals were used to measure rumen fermentation characteristics. In both experiments animal performance was monitored. The inclusion of dietary additives decreased methane emissions (g/d) by 10%. Milk yield and milk fat content tended to be lower for ADD in experiment 1. In experiment 2, milk production was not affected by ADD, but milk fat content was lower. Fat- and protein-corrected milk was lower for ADD in both experiments. Milk urea nitrogen content was lowered by ADD in experiment 1 and tended to be lower in experiment 2. Apparent total tract digestibility of fat, but not that of starch or neutral detergent fiber, was higher for ADD. Energy retention did not differ between treatments. The decrease in methane production (g/d) was not evident when methane emission was expressed per kilogram of milk produced. Feeding ADD resulted in increases of C12:0 and C14:0 and the intermediates of linseed oil biohydrogenation in milk in both experiments. In experiment 2, ADD-fed cows tended to have a decreased number of protozoa in rumen fluid when compared with that in control cows. Total volatile fatty acid concentrations were lower for ADD, whereas molar proportions of propionate increased at the expense of acetate and butyrate.

The chain length of dietary saturated fatty acids affects human postprandial lipemia.

OBJECTIVE: Saturated fats increase total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) and are linked to coronary artery disease risk. The effect of variance in chain length of saturated fatty acids (SFA) on coronary artery disease in human postprandial lipemia is not well elucidated. METHODS: A total of 20 healthy volunteers were challenged with 3 test meals, similar in fat content (~31% en) but varying in saturated SFA content and polyunsaturated/saturated fatty acid ratios (P/S). The 3 meals were lauric + myristic acid-rich (LM), P/S 0.19; palmitic acid-rich (POL), P/S 0.31; and stearic acid-rich (STE), P/S 0.22. Blood was sampled at fasted baseline and 2, 4, 5, 6, and 8 hours. Plasma lipids (triacylglycerol [TAG]) and lipoproteins (TC, LDL-C, high density lipoprotein-cholesterol [HDL-C]) were evaluated. RESULTS: Varying SFA in the test meal significantly impacted postprandial TAG response (p < 0.05). Plasma TAG peaked at 5 hours for STE, 4 hours for POL, and 2 hours for LM test meals. Area-under-the-curve (AUC) for plasma TAG was increased significantly after STE treatment (STE > LM by 32.2%, p = 0.003; STE > POL by 27.9%, p = 0.023) but was not significantly different between POL and LM (POL > LM by 6.0%, p > 0.05). At 2 hours, plasma HDL-C increased significantly after the LM and POL test meals compared with STE (p < 0.05). In comparison to the STE test meal, HDL-C AUC was elevated 14.0% (p = 0.005) and 7.6% (p = 0.023) by the LM and POL test meals, respectively. The TC response was also increased significantly by LM compared with both POL and STE test meals (p < 0.05). CONCLUSIONS: Chain length of saturates clearly mediated postmeal plasma TAG and HDL-C changes.

Control of Listeria monocytogenes by lauric arginate on frankfurters formulated with or without lactate/diacetate.

Listeria monocytogenes (Lm) is a food safety concern that can be associated with ready-to-eat (RTE) meat and poultry products because of its persistence in the processing environment. Listeriosis has a fatality rate of 28% in immuno-compromised individuals. RTE meats receive a lethal heat treatment but may become contaminated by Lm after this treatment. Federal regulators and manufacturers of RTE meats are working to find additional ways to control postprocess contamination by Lm in RTE meats. This research was initiated to validate combinations of antimicrobials that would produce an immediate lethality of at least 1 log of Lm on artificially contaminated frankfurters, and also suppress Lm growth to less than 2 logs throughout the extended shelf life at refrigerated temperatures (4 degrees C). Based on our studies, 22-ppm lauric arginate (LAE, ethyl-N-dodecanoyl-L-arginate hydrochloride) gave more than a 1-log reduction of Lm surface inoculated onto frankfurters within 12 h. The combination of either 1.8%/0.13% or 2.1%/0.15% potassium lactate/sodium diacetate (L/D) in combination with 22 ppm LAE caused more than a 2-log reduction at 12 h. Storage studies revealed that complementary interactions of L/D and LAE also met the 2nd requirement. This combination initially reduced Lm by 2 logs and suppressed growth to less than 2 logs even at the end of the 156-d storage life for frankfurters. These results confirmed that the combination of L/D with LAE as a postprocessing-prepackaging application could be useful in complying with the USDA's Alternative 1 that requires validation for the control of Lm on RTE frankfurters.

[A new rat model of cerebral infarction based on the injury of vascular endothelial cell].

OBJECTIVE: A new rat model of cerebral infarction was developed to elucidate the contribution of vascular endothelial cell during focal cerebral infarction formation. METHODS: Forty-eight Sprague-Dawley (SD) rats were randomly divided into the model group, sham operation group, and control group for indexes observation of triphenyltetrazolium chloride (TTC) dyeing, neurological deficit, plasma tissue-type plasminogen activator (tPA) activity, plasminogen activator inhibitor (PAI) activity, thromboxane B(2) (TXB(2)) content, and 6-keto-prostaglandin (6-keto-PGF(1alpha)) content. RESULTS: (1) The highest neurological score appeared at 6 h after operation, descending significantly at sequential time. (2) Using TTC dyeing and optical microscope technique, pathological changes in brains were observed. (3) Compared with control group and sham operation groups, there was a decrease in tPA activity of model rats at the initial 12 h after injection of sodium laurate (P < 0.05), PAI activity decreased markedly in the model group at 24 h after injection of sodium laurate. (4) In plasma TXB(2) concentration reached the highest level compared at 6 h after injection of sodium laurate, but there were not obvious differences in plasma 6-keto-PGF(1alpha) concentration among all groups (P > 0.05). CONCLUSION: Focal cerebral infarction in rats could be induced by some sodium laurate, showing ischemic cerebrum necrosis, function disorder of vascular endothelium-platelet, fibrinolysis abnormality. This model could play an important role in researching the contribution of vascular endothelial cell during cerebral infarction development, preventing and curing by traditional Chinese medicine.

Digestive and metabolic utilization of lauric, myristic and stearic acid in cows, and associated effects on milk fat quality.

In an experiment with 3 x 6 Brown Swiss cows, the effects of dietary supplementations (40 g/kg) of non-esterified lauric (12 : 0), myristic (14 : 0) and stearic acid (18 : 0) on digestibility, metabolisability, milk fat composition and melting properties were investigated. The diet consisted of forage and concentrate in a ratio of 3 : 2. Cows were fed the C18 : 0 supplemented diet for 10 days before treatment feeding started for a 15-day experimental period where, at the end, excreta were quantitatively collected and gaseous exchange was measured. The DM intake averaged 17.9 kg/d for the C14 : 0 and C18 : 0 diets and was reduced (P < 0.05) by 18% in the C12 : 0 diet. The realised intakes of total C12 : 0, C14 :0 and C18 : 0 amounted to 368, 391 and 617 g/d in the respective groups. The efficiency of ME utilization for lactation was higher (P < 0.001) in the C12 : 0 group than in the two other groups indicating differences in metabolism of C12 : 0 in comparison with C14 : 0 and C18 : 0. Shifts in dietary fatty acid supplementation were clearly reflected in the milk fat composition. Associated changes were elevated CLA and C18 : 1 trans when supplementing C12 : 0, and a high C18 : 1 to C16 : 0 ratio (P < 0.05) in the C12 : 0and C18 : 0 groups which resulted in an easier melting milk fat than with supplementary C14 : 0. Despite certain favourable effects of C12 : 0 in metabolic energy utilization and milk fat melting properties (relative to C14 : 0), more research is needed on how to improve its palatability for dairy cows.

Effect of dietary cholesterol, trans and saturated fatty acids on serum lipoproteins in non-human primates.

Nine cynomolgus monkeys were rotated randomly through four dietary treatments with each treatment lasting 6 weeks. A wash-out period of 4 weeks was maintained between each dietary rotation. The animals were fed diets containing 32% energy fat derived from palm olein (POL), lauric-myristic-rich oil blend (LM), American Heart Association (AHA) rich oil blend and hydrogenated soybean oil blend (trans). Diets were fed with (phase 1) or without (phase 2) the addition of dietary cholesterol (0.1%). In phase 1, when animals were fed without dietary cholesterol, plasma total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) was significantly raised and high-density lipoprotein cholesterol (HDL-C) was significantly depressed by the trans diets relative to all other dietary treatments. The resulting LDL-C/HDL-C ratio was also significantly increased. The LM diet increased TC significantly relative to the AHA diet while LDL-C was significantly increased compared to both POL and AHA. Apolipoprotein (apo) B was not affected significantly by these dietary treatments. Apo A1 was significantly increased by POL relative to all other dietary treatments. The trans diet reduced apo A1 and the resulting apo B/A1 ratio was increased significantly by trans relative to all other dietary treatments. Addition of 0.1% dietary cholesterol to these diets almost doubled the plasma TC and LDL-C in all dietary treatments. However, HDL-C was only marginally higher with the addition of dietary cholesterol. The LM + C (cholesterol added) diet resulted in the highest TC and LDL-C that was significant compared to all other dietary treatments. Trans + C increased TC compared to POL + C and AHA + C diets while increases in the LDL-C did not attain significance. The addition of dietary cholesterol did not affect HDL-C between treatments whereas plasma triglycerides were significantly increased by the trans + C diet relative to all other treatments. Both the trans + C and LM + C diets increased apo B and decreased apo A1 relative to the POL + C and AHA + C diets. The resulting apo B/A1 ratio was similarly altered. These results affirm that the lauric + myristic acid combination, along with trans fatty acids, increased lipoprotein-associated coronary heart disease risk factors compared to either POL or AHA.

Mutations in erg4 affect the sensitivity of Saccharomyces cerevisiae to medium-chain fatty acids.

We have found that the medium-chain fatty acids (MCFAs) undecanoic acid (11:0), 10-undecenoic acid (11:1 Delta 10), and lauric acid (12:0) can affect the growth of Saccharomyces cerevisiae in a dose-dependent manner. The principal effect was a longer lag phase in MCFA-containing medium, although higher concentrations of 11:1 Delta 10 inhibited growth. Their relative order of inhibitory action was 11:1 Delta 10>11:0>12:0. Cellular content with MCFA supplementation was dependent on the concentration and the particular species of fatty acid, with 12:0 showing the highest relative accumulation and 11:1 Delta 10 the lowest at all concentrations. We have isolated and characterized a mutant that is hypersensitive to MCFA supplementation and is unable to grow at the normally permissive condition of 1 mM 11:1 Delta 10. However, it does not appear to accumulate higher relative levels of the fed MCFA compared to wild-type cells. Complementation of the mutant revealed that the ERG4 gene, encoding the enzyme that catalyzes the last step in ergosterol biosynthesis, had been mutated. The fatty acid composition of the erg4 Delta mutant differs only slightly from wild-type cells, mainly involving an increase in the relative amount of 12:0. These results indicate that yeast require ergosterol for optimal growth on certain MCFAs. We discuss the role ergosterol may have in cells responding to exogenous MCFAs and in supporting optimal cell growth.

Consumption of a solid fat rich in lauric acid results in a more favorable serum lipid profile in healthy men and women than consumption of a solid fat rich in trans-fatty acids.

Solid fats are used in food manufacturing to provide texture and firmness to foods. Such fats are rich in either saturated or trans-fatty acids, both of which increase the risk of coronary heart disease. Epidemiological and experimental studies suggest that trans-fatty acids increase risk more than do saturates because they lower serum high density lipoprotein (HDL) cholesterol. However, there appear to be differences between saturates in their effect on HDL cholesterol. We investigated whether the consumption of a solid fat rich in lauric acid (C12:0) would result in a more favorable blood lipid profile than the consumption of a solid fat rich in trans-fatty acids. We fed 32 healthy men and women two controlled diets in a 2 x 4-wk randomized crossover design. The diets consisted of a background diet supplemented with margarines. In the trans-diet, 9.2% of energy was provided by trans-fatty acids and 12.9% by saturated fatty acids. In the Sat-diet, energy intake was 0% from trans-fatty acids and 22.9% from saturated fatty acids. Lauric acid composed one third of all saturates in the Sat-diet. Serum HDL cholesterol was 0.36 mmol/L lower at the end of the trans-diet than at the end of the Sat-diet (95% confidence interval, -0.46 to -0.26), whereas serum low density lipoprotein cholesterol and triglyceride concentrations remained stable. Serum total cholesterol was 0.31 mmol/L (95% confidence interval, -0.48 to -0.14) lower at the end of the trans-diet than at the end of the Sat-diet. Consumption of a solid fat rich in lauric acid gives a more favorable serum lipoprotein pattern than consumption of partially hydrogenated soybean oil rich in trans-fatty acids. Thus, solid fats rich in lauric acids, such as tropical fats, appear to be preferable to trans-fats in food manufacturing, where hard fats are indispensable.

Mechanisms mediating lipoprotein responses to diets with medium-chain triglyceride and lauric acid.

Medium-chain triglycerides (MCT) are often used in specialized formula diets or designer fats because of their special properties. Yet their influence on lipid metabolism is not completely understood. In this two-period cross-over study, the effects of MCT (8:0 + 10:0) in contrast to a similar saturated fatty acid (12:0) were compared. Eighteen healthy women ate a baseline diet [polyunsaturated (PUFA)/saturated fat = 0.9] for 1 wk. Then, they consumed test diets (PUFA/saturated fat = 0.2) for 4 wk. Monounsaturated fat and cholesterol were constant in baseline and treatment diets. MCT and 12:0, substituted for part of the PUFA, provided 14 energy (en)% of the test diets. In comparison to the PUFA baseline diet, a 16% increase in mean serum low density lipoprotein (LDL)-cholesterol (C) on the 12:0 diet was accompanied by a 21% decrease in mean receptor-mediated degradation of LDL by freshly isolated mononuclear cells (MNC) in vitro. The MNC assay theoretically gives an indication of receptor-mediated degradation of LDL. In contrast, the MCT diet raised mean receptor-mediated degradation of LDL by 42%, a finding out of line with the mean 11% increase in serum LDL-C. Perhaps MCT, by increasing the rate of LDL-C production, overcame the rate of LDL-C clearance. The 12:0 diet enhanced some factors involved in reverse cholesterol transport (e.g., high density lipoprotein fractions) while MCT had a different or less pronounced effect. The overall effects of MCT on cholesterol metabolism may or may not be desirable, whereas those of 12:0 appear largely undesirable as previously reported.

Regulation of guinea pig very low density lipoprotein secretion rates by dietary fat saturation.

We investigated the effects of dietary fat saturation on very low density lipoprotein (VLDL) production in guinea pigs fed semipurified diets containing 15% (w/w) fat, either corn oil (CO, 58% linoleic acid), lard (LA, 42% oleic and 24% palmitic acids) or palm kernel oil (PK, 52% lauric and 18% myristic acids) for 4 weeks. Animals were given an intravenous injection of Triton WR 1339 to block VLDL catabolism and rates of VLDL triacylglycerol (TAG) and apolipoprotein (apo) B secretion were measured over time. Plasma TAG concentrations increased linearly for 8 h (r = 0.99) and VLDL-TAG secretion rates were significantly higher (P < 0.01) in guinea pigs fed LA (72.7 +/- 14.7 mg/kg-h, n = 12) compared to animals fed PK (55.4 +/- 13.4 mg/kg-h, n = 12) or CO (48.6 +/- 17.5 mg/kg-h, n = 15). VLDL apoB secretion rates were highest in PK-fed animals (3.1 +/- 1.8 mg/kg-h) compared to guinea pigs fed LA (1.5 +/- 0.8 mg/kg-h) or CO (1.1 +/- 0.6 mg/kg-h) diets (P < 0.005). Concurrent with analysis of VLDL secretion, turnover of 125I-labeled LDL was measured. Low density lipoprotein (LDL) fractional catabolic rates were not altered by Triton treatment and LDL apoB specific radioactivity (cpm/microgram) did not change over time indicating that: a) the Triton blockage of VLDL catabolism was complete, and b) there was no direct secretion of LDL by the liver. These data demonstrate that intake of lard increases the rate of VLDL-triacylglycerol secretion and that nascent VLDL particles from the lard and corn oil diet groups have the same relative triacylglycerol content, whereas palm kernel oil intake increases secretion of VLDL particles which have a reduced triacylglycerol content. These results demonstrate that dietary fat chain length and saturation have specific effects on VLDL secretion rates affecting both particle number and composition.

Immune responses in swine given lipid-conjugated pseudorabies viral antigens.

The immune response was compared in pigs given inactivated pseudorabies virus (PRV) antigens (with or without adjuvant) or PRV antigens covalently conjugated with a fatty acid (lauric acid) to enhance delayed-type hypersensitivity. The pigs were given 2 inoculations, 14 days apart, and were challenge exposed 28 days after the 1st inoculation. Pibs inoculated with PRV antigens, with or without adjuvant, had significant virus-neutralizing (VN) antibodies before challenge exposure, but the pigs inoculated with lipid-conjugated PRV antigens had no detectable VN antibodies, with the exception of 1 pig. All inoculated pigs were positive by the microimmunodiffusion test at postinoculation day 14 and remained positive throughout the experiment. The inoculated pigs had delayed-type hypersensitivity reactions when skin tested a postinoculation day 25; the pigs inoculated with lipid-conjugated PRV antigens had a more pronounced reaction. Inoculated pigs had mild respiratory signs on the 3rd through the 6th days after challange exposure, with no observable difference in severity between the inoculated groups. The control pigs had acute signs of PRV, and 3 or 4 pigs died 5 to 8 days after challenge exposure. The average VN titers of the different inoculated groups of pigs were nearly equal 2 weeks after challenge exposure. Results indicated that both humoral antibodies and cell-mediated immunity have a role in PRV infections in swine.