No description available.

The negative health effects of trans fatty acids from hydrogenated fats on plasma lipid profile have been well documented. However, the mechanisms responsible for these changes remain to be elucidated. Hence the overall objective of the thesis was to examine the effect of consuming different forms of hydrogenated fats on cholesterol and triglyceride metabolism, specifically fractional and absolute synthesis rates of free (FSR-FC and ASR-FC) and esterified (FSR-CE, AER and ER) cholesterol, and the functioning of the ASP pathway. In addition, validation of the newer deuterium incorporation (DI) method for measurement of endogenous cholesterol biosynthesis against the cholesterol precursor assessment approach was also performed. Fourteen moderately hypercholesterolemic (LDL-C ≥ 130 mg.dl-1) postmenopausal women (65--71yrs) participated in this study. Subjects consumed, in random order, each of 6 diets for 5 week periods, separated by washout periods ranging from 2 to 4 weeks in duration. The experimental diets included a baseline (BL) diet (39% kcal fat) and 5 reduced fat diets (30% kcal) where 2/3rd of the fat was either soybean oil (SO), low trans squeeze (SQM), medium trans tub (TM), high trans stick (SM) margarines, or butter (BT). Results obtained from the series of analyses performed demonstrate that: (i) the DI method and levels of some cholesterol precursors correspond as methods for the study of in vivo cholesterol biosynthesis in humans; (ii) elevations in endogenous cholesterol synthesis (FSR-FC and ASR-FC) are not responsible for the increase in circulating cholesterol levels seen after consumption of the high trans SM, and high SFA rich BT and BL diets; (iii) suppression of cholesterol esterification rates on the SM diet may account for the decreased HDL-C levels observed on this diet and finally; (iv) dysfunction of the ASP pathway, with lower ASP and higher FFA levels could be responsible for the higher secretion of hepatic B 100 particles. In conc

In a cross-sectional study we examined Iipoprotein composition and CETP mass in 15 sedentary and 12 exercising, healthy male volunteers, aged between 17-35 years. The exercising group were defined as individuals participating in at least five weekly 45 minute exercise sessions of an aerobic nature (60-85% estimated maximal oxygen uptake). The sedentary subjects were only irregularly engaged in bouts of physical activity, not more than 45 minutes per week. Seasonal data were collected: one data collection in the fall and one in the spring. A 20 day food and exercise journal was maintained during each season's data collection period. Blood lipids were measured on two and anthropometric and aerobic capacity testing were performed on 1 occasion during each season. Statistical analyses consisted of a two way ANOVA (exercise and season) to control for seasonal effects on blood lipids and Iipoprotein levels. Pearson product moment correlations were calculated between those variables that showed significant seasonal or level of activity changes. Exercising males consumed significantly greater amounts of energy (p<O.OOI), carbohydrates (p<O.OOOI), protein (p<O.OOOI), and dietary fibre (p<O.OOOI) than sedentary males; sedentary males however, consumed significantly greater amounts of alcohol than exercising males. Exercising males had significantly higher aerobic capacities and degrees of mesomorphy than sedentary subjects and exhibited significantly lower apo AI values. No differences were noted between the 2 groups in BMI, % body fat, other plasma lipids or CETP mass. In summary, regular physical activity in young, healthy male subjects was associated with increased energy and carbohydrate intake and improved aerobic capacity as compared to sedentary subjects. Moderate differences in physical activity were not however associated with alterations in plasma Iipoprotein composition or CETP concentration.

Absence of stearoyl-CoA desaturase-1 (SCD1) in mice leads to chronic inflammation of the skin and increased susceptibility to atherosclerosis, while also increasing plasma inflammatory markers. A recent report suggested that SCD1 deficiency also increases disease severity in a mouse model of inflammatory bowel disease, induced by dextran sulfate sodium (DSS). However, SCD1-deficient mice are known to consume increased amounts of water, which would also be expected to increase the intake of DSS-treated water. The aim of this study was to determine the effect of SCD1 deficiency on DSS-induced acute colitis with DSS dosing adjusted to account for genotype differences in fluid consumption. Wild-type controls were treated with 3.5% DSS for 5 days to induce moderately severe colitis, while the concentration of DSS given to SCD1-deficient mice was lowered to 2.5% to control for increased fluid consumption. Colonic inflammation was assessed by clinical and histological scoring. Although SCD1-deficient mice consumed a total intake of DSS that was greater than that of wild-type controls, colonic inflammation, colon length and fecal blood were not altered by SCD1-deficiency in DSS-induced colitis, while diarrhea and total weight loss were modestly improved. Despite SCD1 deficiency leading to chronic inflammation of the skin and increased susceptibility to atherosclerosis, it does not accelerate inflammation in the DSS-induced model of acute colitis when DSS intake is controlled. These observations suggest that SCD1 deficiency does not play a significant role in colonic inflammation in this model. [The original version of this article, along with updated information and services is located on the World Wide Web at: http://dx.doi.org/10.1016/j.bbalip.2009.08.001]

Assembly of intestinal chylomicron particles (lipid-protein complexes) is the fundamental mechanism by which we absorb dietary fat. Two intestinal lipid transporters, Cluster of Differentiation 36 (CD36) and fatty acid-binding protein 1 (FABP1), have been shown to play a role in lipid absorption, however, it remains unclear how knockdown of these proteins bleads to aberrant intestinal chylomicron secretion. In an enterocyte-like cell culture model, Caco-2 cells, we hypothesized that knockdown of CD36 or FABP1 using short-hairpin RNA interference techniques would impair triacylglycerol (TG) and apolipoprotein B (apoB) secretion. Surprisingly, knockdown of these lipid transporters lead to an increase in TG and apoB secretion that was associated with an increase in fatty acid synthase and fatty acid transport protein 4 (FATP4) protein levels. De novo fatty acid synthesis was slightly increased in CD36-, but not FABP1-knockdown Caco-2 cells. This study highlights the importance of fatty acid targeting in regulating chylomicron production.

Assembly of intestinal chylomicron particles (lipid-protein complexes) is the fundamental mechanism by which we absorb dietary fat. Two intestinal lipid transporters, Cluster of Differentiation 36 (CD36) and fatty acid-binding protein 1 (FABP1), have been shown to play a role in lipid absorption, however, it remains unclear how knockdown of these proteins bleads to aberrant intestinal chylomicron secretion. In an enterocyte-like cell culture model, Caco-2 cells, we hypothesized that knockdown of CD36 or FABP1 using short-hairpin RNA interference techniques would impair triacylglycerol (TG) and apolipoprotein B (apoB) secretion. Surprisingly, knockdown of these lipid transporters lead to an increase in TG and apoB secretion that was associated with an increase in fatty acid synthase and fatty acid transport protein 4 (FATP4) protein levels. De novo fatty acid synthesis was slightly increased in CD36-, but not FABP1-knockdown Caco-2 cells. This study highlights the importance of fatty acid targeting in regulating chylomicron production.

No description available.

The overall objective of this study was the optimization of a model enzymatic system in organic solvent media for the biosynthesis of selected phenolic lipid compounds. The model enzymatic system consisted of cinnamic acid and oleyl alcohol as substrates using commercial immobilized lipase (Novozym 435) from Candida antarctica. The experimental findings showed that an increase in the hydrophobicity of the solvent mixture and a decrease in the aw values of the reaction medium increased the initial enzymatic activity and bioconversion yield; the use of an iso-octane and butanone solvent mixture (85:15, v/v) and an initial aw of 0.05 resulted in an initial enzymatic activity of 192.7 nmol product/g enzyme/min and a corresponding bioconversion yield of 95.3% after a 16-day reaction period.

Fourier transform infrared (FTIR) spectroscopy was employed to monitor the oxidation of edible oils in the absence and presence of antioxidants. Three synthetic antioxidants (butylated hydroxyanisole, propyl gallate and tert-butylhydroxyquinone) were added to menhaden oil at three different concentrations (1%, 0.1%, and 0.01%), and the FTIR spectra of the oils under conditions of oxidative stress were recorded as a function of time. The efficacy of each antioxidant was assessed by monitoring bands at 3444 cm$ sp{-1}$, characteristic of hydroperoxide formation, 971 cm$ sp{-1}$ for trans double bond formation, and 3008 cm$ sp{-1}$ for cis depletion. An FTIR spectroscopic method was also developed for the determination of the peroxide value of edible oils undergoing oxidation, based on the measurement of the 3444-cm$ sp{-1}$ band. The results of the FTIR method were compared to those from both the iodometric chemical method and the enzymatic hemoglobin-methylene blue assay for the determination of hydroperoxide content. The FTIR predictions were within $ pm$3% of the values obtained by both the chemical and the enzymatic method. Finally, the determination of the hydroxyl value of emulsifiers by FTIR spectroscopy was investigated. Both attenuated total reflectance (ATR) and transmission flow cell techniques were used to record the spectra of commercial monoglycerides. Calibration models for the prediction of hydroxyl value from the FTIR spectra were developed using partial-least-squares (PLS) regression for both the ATR and transmission spectra. Cross-validation of the calibration models yielded an overall average error in the predicted hydroxyl values of $ sim$3% for both the ATR and transmission flow cell methodologies. Linear regression of the FTIR-predicted versus the hydroxyl values determined by the reference chemical method yielded r = 0.998 for the ATR and r = 0.997 for the transmission flow cell method.

Dietary fats and animal proteins have been shown to exert different lipidemic responses in many animals, including humans. Oxidative stress has been associated with the development of several diseases including atherosclerosis. The hypotheses of this study were that: (1) the degree and type of dietary fatty acid unsaturation will influence the type of cholesterolemic responses via the induction of differential levels of oxidative stress; and (2) hyperlipidemia induced by casein in a butterfat-based diet is related to increased tissue lipid peroxidation. Male Golden Syrian hamsters were fed diets containing butterfat/casein (BF/CAS), butterfat/egg white (BF/EGG), safflower oil/egg white (SAFF/EGG) or menhaden oil/egg white (MHO/EGG) for 27 days. In comparison to the BF/EGG and SAFF/EGG diet groups, the MHO/EGG hamsters exhibited higher levels of total serum cholesterol, serum triglyceride, serum apolipoprotein B and serum lipid peroxides. These results suggest that MHO induced-hyperlipidemia could be exerted through increased concentrations of serum apolipoprotein B and increased serum lipid peroxidation. The BF/CAS diet, in comparison to the BF/EGG diet, increased serum total cholesterol and increased serum and hepatic levels of lipid peroxides. These results suggest that dietary casein-induced hypercholesterolemia could be related to increased oxidative stress. The protective effect of dietary egg white on lipid peroxidation may involve sulfur amino acids which are found in greater amounts in egg white than casein.