No description available.

No description available.

Dietary fatty acids are precursors of the lipid mediator group of compounds termed fatty acid ethanolamides (FAE). Prolonged intake of specific types of dietary fats has been shown to increase FAE levels. However, the short term effects of qualitative dietary fat intake on FAE levels remain understudied. Hence, the objective of this study was to identify the effect of diets containing varying concentrations of n-9 from canola oil (CO) and n-3 fatty acids from DHA rich oil (DRO) on plasma and organ FAE levels after different time points in male Sprague Dawley rats. Sixty-four rats were randomly assigned into four groups and were fed diets containing 40% as energy of either safflower, 95% CO: 5% DRO, 50% CO: 50% DRO and 5% CO: 95% DRO. These diets were consumed within a 2hr window in all groups. Circulating fatty acid and FAE levels were measured at 3, 6, 12 and 24hr within each group. At 3hr, significant differences (p<0.05) in plasma oleoylethanolamide (OEA) levels were seen in the 95% CO group: 5% DRO group and 5% CO group: 95% DRO group as well as between 50% canola oil group: 50% DRO and 5% CO group: 95% DRO. In all dietary groups, palmitoylethanolamide (PEA) levels were not significantly different at 3, 6 and 24hr compared to 0hr, but did at 12hr where the 50% CO:50% DRO group showed significantly lower levels than seen in the 95% CO group, but PEA levels were not different from the 5% canola oil group. Although plasma FAE levels were generally multiple times lower than observed in small intestine, liver or brain, arachidonoylethanolamide (AEA) levels were significantly lower in the 95% DRO group than in the remaining two groups. Plasma docosahexanoylethanolamide (DHEA) showed no difference across all time points except at 24hr where levels were higher (p<0.05) in the 95% DRO group than in the remaining two groups. In liver at 3hr, OEA levels were higher (p<0.05) in the 95% CO group than the groups with lesser concentrations of oleic acid, while liver OEA levels showed no difference at any other time points across dietary groups. LEA levels were higher in 95% CO: 5% DRO group compared to the 5% CO group: 95% DRO group after 3hr of feeding. Liver DHEA levels were observed to be highest in the 5% CO group: 95% DRO group at 3 and 12, but not at 6 or 24hr. The dietary fatty acid composition affects plasma and organ fatty acid profiles in a time dependent manner and also produces time shifts in plasma and organ FAE levels. These dietary induced changes according to time points in the levels of FAEs may translate into discernible changes in energy expenditure and lipid levels which may in turn influence the risk of obesity. / February 2017

Understanding the movement and feeding habits of marine animals is crucial when managing their populations. The molecular, and stable carbon isotope composition of fatty acids from an organism provides time-integrated information on its dietary intake. Hence, when spatial differences in the quality of seston exist it should be able to trace these differences up into higher trophic level organisms. The presented study evaluates the applicability of 13C/12C ratios of individual fatty acids, as natural tags and dietary markers in marine pelagic organisms. In addition, the use of 13C/12C ratios of bulk sample, as well as fatty acid composition data in examining the movement, and diet of animals are further explored. Samples of particulate organic matter, zooplankton, larval fish and juvenile salmon collected during three cruises off the west coast of Vancouver Island were analyzed. The fatty acid composition, stable carbon isotope ratio of either bulk sample, or individual fatty acids could typically distinguish samples collected in continental shelf waters from off-shelf samples. The differences in fatty acid composition between the adjoining food webs seem to be mainly caused by the different contribution of diatom-derived material to the base of the food web. The higher 13C/12C ratios found in the diatom-richer seston in shelf waters were not simply caused by the higher contribution of diatoms. Instead, stable carbon isotope data on individual fatty acids indicate that growth conditions favouring diatom growth caused 13C-enrichment in algae other than diatoms as well. The relative abundance of polyunsaturated fatty acids, such as docosahexaenoic acid (22:6n-3), were found to increase with trophic level. Whereas the abundance of saturated, and monounsaturated fatty acids was higher in organisms from lower trophic levels. This suggests that the fatty acid composition may be a useful trophic level indicator. However, literature data indicate that these trends observed in seston. zooplankton, larval fish and juvenile salmon, do not hold for larger organisms and adult life stages. / Graduate

No description available.

Basic and clinical research documents the benefits of dietary milled flaxseed (MFX), a rich source of alpha-linolenic acid (ALA) and lignans, in the attenuation of risk factors key to regulating cardiovascular disease (CVD) progression. ALA has antihypertensive properties and the lignan metabolites, enterodiol (END) and enterolactone (ENL), have antioxidative potential. The effectiveness of these bioactives to reduce risk factors of CVD may be dependent upon their plasma concentrations. To study this, we first designed and validated a method using supported liquid extraction and gas chromatography/mass spectrometry to isolate and quantify enterolignans in plasma. Applying this technique, we examined MFX doses of 10-40 g/d administered to healthy, younger adults (18-49 years of age) for 4 weeks. Ten g/d was sufficient to significantly increase circulating ALA (1.5 fold) and enterolignans (5-31 fold). There was no significant dose-dependent response. In another investigation, younger (18-29 years of age) and older (45-69 years of age) healthy adults were studied to determine if age influenced enterolignan metabolism. CVD is associated with advanced age but older people may not be able to obtain lignan metabolites from dietary MFX. Following 4 weeks of MFX consumption, both age groups increased plasma total enterolignans (END + ENL) with no between-group differences. This suggested that older and younger adults metabolize MFX lignans equally. A final study assessed MFX bioactives in plasma of peripheral artery disease patients >40 years of age. Plasma enterolignans increased 10-50 fold and ALA 1-2 fold after only one month of MFX ingestion. Dietary MFX also attenuated total (11%) and LDL (15%) cholesterol in these patients after 1-6 months of administered MFX compared to placebo. The attenuation in cholesterol was due to the high fiber content of flaxseed, and not to ALA and enterolignans, despite their marked increase in circulation. MFX did not interfere with cholesterol-lowering medications but instead decreased cholesterol levels beyond the effects of medications alone. To conclude, dietary supplementation with MFX resulted in an increase in plasma enterolignan and ALA concentrations in healthy younger and older adults and in patients with pre-existing CVD. The cholesterol-lowering benefits of MFX were additional to cholesterol-lowering drugs and likely attributed to MFX fiber. / May 2016

A thesis submitted to the Faculty of Medicine, University o-f the Witwatersrand, Johannesburg, ■for the degree o-f Master o-f Science. Johannesburg, 1990. / In this thesis the role of essential fatty acids (EFAs) in thermoregulation and the polyunsaturates (PUFA) in the genesis of fever is investigated. Although recognised, that metabolites of arachidonic acid are involved in the biochemical sequences leading to fever, it is also acknowledged that fever response depends on lipid mobilisation. However, the exact biochemical mechanisms involved in this event remain unknown to date. In order to investigate a relation between serum lipids and fever, rabbits were subjected to dietary manipulation (deficient, or excessive EFA diet) and their hyperthermic responses to intravenous injections of (a) human leucocyte pyrogen (HLP); (b) endotoxin (Salmonella Thyphosa); and (c) cerebroventricular injections of prostaglandin E2» were compared with rabbits fed on a normal diet / IT2018

IT2018

David Chi-cheong Wan. / Bibliography: leaves 75-85 / Thesis (M.Ph.)--Chinese University of Hong Kong, 1984

by Sea Man Mei, Mandy. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1998. / Includes bibliographical references (leaves 203-214). / Abstract also in Chinese. / ACKNOWLEDGMENTS --- p.i / ABSTRACT --- p.ii / LIST OF ABBREVAIATIONS --- p.vi / TABLE OF CONTENTS --- p.vii / Chapter Chapter1 --- General Introduction / Chapter 1.1 --- DEFINITION --- p.2 / Chapter 1.2 --- MOTIVATION OF THE ONSET OF WEIGHT CYCLING --- p.3 / Chapter 1.3 --- PHYSIOLOGICAL EFFECTS OF WEIGHT CYCLING --- p.6 / Chapter 1.3.1 --- """Dieting-Induced Obesity"" Hypothesis" --- p.6 / Chapter 1.3.1.1 --- Food Efficiency --- p.6 / Chapter 1.3.1.2 --- Proposed Mechanisms for the Increase of Food Efficiency --- p.10 / Chapter 1.3.1.3 --- Change in Body Fat --- p.14 / Chapter 1.3.2 --- Association with Increased Mortality and Coronary Heart Disease (CHD) --- p.15 / Chapter Chapter2 --- Depletion of Linoleic Acid and α-Linolenic Acid Caused by Weight Cycling is Independent of the Extent of Calorie-Restriction / Chapter 2.1 --- INTRODUCTION --- p.18 / Chapter 2.1.1 --- Nomenclature of Fatty Acids --- p.18 / Chapter 2.1.2 --- Metabolism and Physiological Roles of LA and α-LnA --- p.19 / Chapter 2.1.2.1 --- "LA, α-LnA and their Derivatives as Structural Components" --- p.21 / Chapter 2.1.2.2 --- Production of Eicosanoids from LA and α-LnA --- p.22 / Chapter 2.1.2.3 --- Other Physiological Roles --- p.23 / Chapter 2.1.3 --- Dietary LA and α-LnA Relative to CHD --- p.24 / Chapter 2.1.3.1 --- Dietary LA and CHD --- p.24 / Chapter 2.1.3.2 --- Dietary α-LnA and CHD --- p.26 / Chapter 2.1.4 --- WC-Induced Alteration in the Composition of Tissue Lipids --- p.27 / Chapter 2.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.29 / Chapter 2.3 --- MATERIALS AND METHODS --- p.30 / Chapter 2.3.1 --- Animals and Diets --- p.30 / Chapter 2.3.2 --- Lipid Analysis --- p.32 / Chapter 2.3.3 --- Triacylglycerol Species Analysis --- p.34 / Chapter 2.3.4 --- Other Assays --- p.35 / Chapter 2.3.5 --- Statistics --- p.35 / Chapter 2.4 --- RESULTS --- p.36 / Chapter 2.4.1 --- Food Intake --- p.36 / Chapter 2.4.2 --- Change of Body weight --- p.38 / Chapter 2.4.3 --- Weight of Liver and Adipose Tissues --- p.40 / Chapter 2.4.4 --- Serum Cholesterol and Triglycerides --- p.41 / Chapter 2.4.5 --- Carcass Total Fatty Acids --- p.42 / Chapter 2.4.6 --- Adipose Tissue Fatty Acids --- p.44 / Chapter 2.4.7 --- Liver Fatty Acids --- p.47 / Chapter 2.5 --- DISSCUSION --- p.50 / Chapter Chapter3 --- Influence of Dietary Fat Level on Fatty Acid Composition and Adiposity in Weight-Cycled Rats / Chapter 3.1 --- INTRODUCTION --- p.56 / Chapter 3.1.1 --- Fat Preference and Intake in Humans --- p.56 / Chapter 3.1.2 --- Alteration of Lipid Metabolism Induced by Dietary Fat --- p.58 / Chapter 3.1.3 --- Interaction Between Weight Cycling and Fat Intake --- p.60 / Chapter 3.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.62 / Chapter 3.3 --- MATERIALS AND METHODS --- p.63 / Chapter 3.3.1 --- Animals and Diets --- p.63 / Chapter 3.3.2 --- Analysis of Adipocytes --- p.66 / Chapter 3.3.3 --- Fatty Acid Analysis --- p.67 / Chapter 3.3.4 --- "Determination of Serum Cholesterol, Triglycerides and Glucose" --- p.68 / Chapter 3.3.5 --- Statistics --- p.68 / Chapter 3.4 --- RESULTS --- p.69 / Chapter 3.4.1 --- Body Weight --- p.69 / Chapter 3.4.2 --- Food Intake and Food Efficiency --- p.71 / Chapter 3.4.3 --- Weight of Liver --- p.74 / Chapter 3.4.4 --- Weight of Adipose Tissue --- p.74 / Chapter 3.4.5 --- Number and Size of Adipocytes --- p.81 / Chapter 3.4.6 --- "Serum Triglycerides, Cholesterol and Glucose" --- p.85 / Chapter 3.4.7 --- Fatty Acid Composition --- p.92 / Chapter 3.5 --- DISCUSSION --- p.145 / Chapter 3.5.1 --- Weight Cycling-Induced Obesity Only with a High-Fat Diet --- p.145 / Chapter 3.5.1.2 --- Effect of Weight Cycling on the Size of Adipocytes --- p.147 / Chapter 3.5.1.3 --- Food Efficiency during Weight Cycling --- p.148 / Chapter 3.5.2 --- Weight-Cycling Induced Specific Alteration of Fatty Acid Metabolism --- p.149 / Chapter Chapter4 --- Weight Cycling Altered the Activities of Lipoprotein Lipase and Lipogenic Enzymes in Rats / Chapter 4.1 --- INTRODUCTION --- p.152 / Chapter 4.1.1 --- Fatty Acid Metabolism --- p.152 / Chapter 4.1.1.1 --- Fatty Acid Synthesis --- p.152 / Chapter 4.1.1.2 --- Fatty Acid Storage --- p.155 / Chapter 4.1.1.3 --- Fatty Acid Oxidation --- p.156 / Chapter 4.1.2 --- Hormonal Control of Fatty Acid Metabolism During Fasting and Refeeding --- p.158 / Chapter 4.1.2.1 --- Fatty Acid Metabolism During Fasting --- p.158 / Chapter 4.1.2.2 --- Fatty Acid Metabolism During Fed-State --- p.160 / Chapter 4.2 --- OBJECTIVE OF THE PRESENT STUDY --- p.161 / Chapter 4.3 --- MATERIALS AND METHODS --- p.162 / Chapter 4.3.1 --- Samples --- p.162 / Chapter 4.3.2 --- Enzymatic Analysis --- p.162 / Chapter 4.3.2.1 --- Lipoprotein Lipase (LPL; EC 3.1.1.34) --- p.162 / Chapter 4.3.2.2 --- Fatty Acid Synthase (FAS; EC 2.3.1.85) --- p.165 / Chapter 4.3.2.3 --- Malic Enzyme (ME; EC 1.1.1.40) --- p.166 / Chapter 4.3.2.4 --- Pyruvate Kinase (PK; EC 2.7.1.40) --- p.166 / Chapter 4.3.2.5 --- Acetyl-CoA Carboxylase (ACC; EC 6.4.1.2) --- p.167 / Chapter 4.3.2.6 --- "Phosphoenolpyruvate Carboxykinase (PEPCK, EC 4.1.1.32)" --- p.168 / Chapter 4.3.2.7 --- Determination of Protein Content --- p.169 / Chapter 4.3.3 --- Determination of Serum Insulin and Serum Glucagon --- p.169 / Chapter 4.3.4 --- Statistics --- p.169 / Chapter 4.4 --- RESULTS --- p.170 / Chapter 4.4.1 --- Enzymatic Analysis --- p.170 / Chapter 4.4.1.1 --- Lipoprotein Lipase --- p.170 / Chapter 4.4.1.2 --- Fatty Acid Synthase --- p.175 / Chapter 4.4.1.3 --- Malic Enzyme --- p.182 / Chapter 4.4.1.4 --- Pyruvate Kinase --- p.182 / Chapter 4.4.1.5 --- Acetyl-CoA Carboxylase --- p.187 / Chapter 4.4.1.6 --- Phosphoenolpyruvate Carboxykinase --- p.187 / Chapter 4.4.2 --- Level of Serum Insulin and Glucagon --- p.192 / Chapter 4.5 --- DISCUSSION --- p.196 / Chapter 4.5.1 --- Effect of Weight Cycling on Activity of Lipoprotein Lipase and Lipogenic Enzymes Activity --- p.196 / Chapter 4.5.2 --- The Overshoot of Enzymatic Activities in Relation to Tissue Fatty Acid Composition --- p.198 / Chapter 4.5.3 --- No Elevation of Plasma Insulin in Weight Cycled Rats --- p.199 / Chapter Chapter5 --- Conclusion --- p.200 / References --- p.203