Thesis (M.Sc.). / Title from title page of PDF (viewed 2008/01/30). Written for the School of Dietetics and Human Nutrition, Macdonald College. Includes bibliographical references.

Lam, Cheuk Kai. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2007. / Includes bibliographical references (leaves 148-173). / Abstracts in English and Chinese. / ACKNOWLEDGEMENTS --- p.i / ABSTRACT --- p.ii / LIST OF ABBREVIATIONS --- p.vi / TABLE OF CONTENTS --- p.x / Chapter CHAPTER 1 --- GENERAL INTRODUCTION / Chapter 1.1 --- Introduction to Cholesterol and Its Related Diseases --- p.1 / Chapter 1.1.1 --- Chemistry of cholesterol --- p.1 / Chapter 1.1.2 --- Physiological importance of cholesterol --- p.1 / Chapter 1.1.3 --- Pathological effects of cholesterol --- p.3 / Chapter 1.1.3.1 --- Mechanism of atherosclerosis --- p.3 / Chapter 1.2 --- Cholesterol Homeostasis --- p.6 / Chapter 1.2.1 --- Liver as the main organ for cholesterol metabolism --- p.6 / Chapter 1.2.2 --- Regulatory sites of cholesterol metabolism --- p.6 / Chapter 1.2.2.1 --- Regulation of cholesterol absorption by acyl coenzyme A: cholesterol acyltransferase (ACAT) --- p.6 / Chapter 1.2.2.2 --- Sterol regulatory element-binding protein 2 (SREBP-2) as a transcription factor for 3 -hydroxy-3 -methylglutaryl coenzyme A reductase (HMGR) and low-density lipoprotein receptor (LDLR) --- p.10 / Chapter 1.2.2.3 --- Roles ofLDLR --- p.11 / Chapter 1.2.2.4 --- Rate limiting role of HMGR in cholesterol de novo synthesis --- p.14 / Chapter 1.2.2.5 --- Roles of liver-X-receptor-a (LXR-a) in cholesterol catabolism --- p.16 / Chapter 1.2.2.6 --- Roles of CYP7A1 in catabolism of cholesterol into bile acids --- p.19 / Chapter 1.2.2.7 --- Roles of cholesterol ester transfer protein (CETP) in maintaining cholesterol distribution in blood --- p.22 / Chapter CHAPTER 2 --- EFFECT OF OCTADECAENOIC ACIDS ON BLOOD CHOLESTEROL IN HAMSTERS / Chapter 2.1 --- Introduction --- p.25 / Chapter 2.1.1 --- Effects of polyunsaturated fatty acids (PUFAs) on blood cholesterol --- p.25 / Chapter 2.1.2 --- Differential effects of 18-C PUFAs on lowering blood cholesterol in vivo --- p.25 / Chapter 2.1.3 --- "Structures, metabolism and conjugation of octadecaenoic acids (ODA)" --- p.26 / Chapter 2.1.4 --- Objectives --- p.26 / Chapter 2.2 --- Experiment 1 --- p.28 / Chapter 2.2.1 --- Materials and methods --- p.28 / Chapter 2.2.1.1 --- Experimental fatty acids --- p.28 / Chapter 2.2.1.1.1 --- Isolation of LN from flaxseed --- p.28 / Chapter 2.2.1.1.2 --- Isolation of CLN from tung seed --- p.28 / Chapter 2.2.1.2 --- Animals --- p.29 / Chapter 2.2.1.3 --- Diets --- p.30 / Chapter 2.2.1.4 --- Plasma lipid measurements --- p.30 / Chapter 2.2.1.5 --- Plasma CETP activity measurement --- p.30 / Chapter 2.2.1.6 --- "Measurement of liver SREBP-2, LDLR, HMGR and CYP7A1 protein abundance by Western blotting" --- p.34 / Chapter 2.2.1.7 --- "Measurement of hepatic SREBP-2, LDLR, HMGR, LXR, CYP7A1, CETP, SR-B1 and LCAT mRNA by real time PCR" --- p.35 / Chapter 2.2.1.7.1 --- Extraction of mRNA --- p.35 / Chapter 2.2.1.1.2 --- Complementary DNA synthesis --- p.36 / Chapter 2.2.1.7.3 --- Real-time polymerase chain reaction (PCR) anaylsis --- p.36 / Chapter 2.2.1.8 --- Determination of cholesterol in liver --- p.37 / Chapter 2.2.1.9 --- Determination of fecal neutral and acidic sterols --- p.38 / Chapter 2.2.1.9.1 --- Determination of fecal neutral sterols --- p.39 / Chapter 2.2.1.9.2 --- Determination of fecal acidic sterols --- p.41 / Chapter 2.2.1.10 --- Statistics --- p.43 / Chapter 2.2.2 --- Results --- p.44 / Chapter 2.2.2.1 --- Growth and food intake --- p.44 / Chapter 2.2.2.2 --- Organ weights --- p.44 / Chapter 2.2.2.3 --- "Effects of ODA on serum TC, TG and HDL-C" --- p.44 / Chapter 2.2.2.4 --- Effect of ODA on liver cholesterol --- p.48 / Chapter 2.2.2.5 --- Effect of ODA on fecal neutral sterol output --- p.48 / Chapter 2.2.2.6 --- Effect of ODA on fecal acidic sterol output --- p.48 / Chapter 2.2.2.7 --- Effect of ODA on cholesterol balance in hamsters --- p.52 / Chapter 2.2.2.8 --- Effect of ODA on plasma CETP activity --- p.52 / Chapter 2.2.2.9 --- Correlation between blood TC and liver cholesterol --- p.52 / Chapter 2.2.2.10 --- Correlation between blood HDL-C and liver cholesterol --- p.52 / Chapter 2.2.2.11 --- Correlation between blood nHDL/HDL ratio and liver cholesterol --- p.52 / Chapter 2.2.2.12 --- Effect ofODA on liver SREBP-2 immunoreactive mass --- p.58 / Chapter 2.2.2.13 --- Effect of ODA on liver LDLR immunoreactive mass --- p.58 / Chapter 2.2.2.14 --- Effect of ODA on liver HMGR immunoreactive mass --- p.58 / Chapter 2.2.2.15 --- Effect of ODA on liver LXR immunoreactive mass --- p.58 / Chapter 2.2.2.16 --- Effect of ODA on liver CYP7A1 immunoreactive mass --- p.63 / Chapter 2.2.2.17 --- Effects ofODA on hepatic CETP mRNA --- p.65 / Chapter 2.2.2.18 --- Effects of ODA on hepatic LDLR mRNA --- p.65 / Chapter 2.2.2.19 --- Effects of ODA on hepatic LXR mRNA --- p.65 / Chapter 2.2.2.20 --- Effects of ODA on hepatic CYP7A1 mRNA --- p.65 / Chapter 2.3 --- Experiment 2 --- p.70 / Chapter 2.3.1 --- Materials and Methods --- p.70 / Chapter 2.3.1.1 --- Experimental diets --- p.70 / Chapter 2.3.1.2 --- Animals --- p.70 / Chapter 2.3.1.3 --- Intestinal acyl coenzyme A: cholesterol acyltransferase (ACAT) activity measurement --- p.70 / Chapter 2.3.1.3.1 --- Preparation of intestinal microsome --- p.71 / Chapter 2.3.1.3.2 --- ACAT activity assay --- p.71 / Chapter 2.3.2 --- Results --- p.73 / Chapter 2.3.2.1 --- Growth and food intake --- p.73 / Chapter 2.3.2.2 --- Organ weights --- p.73 / Chapter 2.3.2.3 --- "Effect of ODA on serum TC, TG and HDL-C" --- p.73 / Chapter 2.3.2.4 --- Effect of ODA feeding on fecal neutral sterol content --- p.77 / Chapter 2.3.2.5 --- Effect of ODA feeding on fecal acidic sterol content --- p.77 / Chapter 2.3.2.6 --- Effect of ODA feeding on intestinal acyl coenzyme A: acyl cholesterol transferase (ACAT) activity --- p.77 / Chapter 2.4 --- Discussion --- p.81 / Chapter CHAPTER 3 --- EFFECT OF OCTADECAENOIC ACIDS ON CHOLESTEROL-REGULATING GENES IN HepG2 / Chapter 3.1 --- Introduction --- p.86 / Chapter 3.1.1 --- HepG2 as a model of cholesterol regulation --- p.86 / Chapter 3.1.2 --- Effect of polyunsaturated fatty acids (PUFAs) on cholesterol regulating genes in cultured cells --- p.87 / Chapter 3.1.3 --- Objectives --- p.89 / Chapter 3.2 --- Materials and Methods --- p.90 / Chapter 3.2.1 --- Cell culture --- p.90 / Chapter 3.2.2 --- "Measurement of SREBP-2, LDLR, HMGR and CYP7A1 protein abundance by Western blotting" --- p.92 / Chapter 3.2.3 --- "Measurement of cellular SREBP-2, LDLR, HMGR, LXR, CYP7A1 and CETP mRNA by real time PCR" --- p.93 / Chapter 3.2.4 --- Statistics --- p.93 / Chapter 3.3 --- Results --- p.95 / Chapter 3.3.1 --- Effect of ODA on HepG2 SREBP-2 immunoreactive mass --- p.95 / Chapter 3.3.2 --- Effect of ODA on HepG2 HMGR immunoreactive mass --- p.95 / Chapter 3.3.3 --- Effect of ODA on HepG2 LDLR immunoreactive mass --- p.95 / Chapter 3.3.4 --- Effect of ODA on HepG2 LXR immunoreactive mass --- p.95 / Chapter 3.3.5 --- Effect of ODA on HepG2 CYP7A1 immunoreactive mass --- p.96 / Chapter 3.3.6 --- Effect of ODA supplementation on HepG2 SREBP-2 mRNA expression --- p.102 / Chapter 3.3.7 --- Effect of ODA supplementation on HepG2 SREBP-2 mRNA expression --- p.102 / Chapter 3.3.8 --- Effect of ODA supplementation on HepG2 LDLR mRNA expression --- p.102 / Chapter 3.3.9 --- Effect of ODA supplementation on HepG2 LXR mRNA expression --- p.106 / Chapter 3.3.10 --- Effect of ODA supplementation on HepG2 CYP7A1 mRNA expression --- p.106 / Chapter 3.3.11 --- Effect of ODA supplementation on HepG2 CETP mRNA expression --- p.106 / Chapter 3.4 --- Discussion --- p.110 / Chapter CHAPTER 4 --- EFFECT OF APPLE POLYPHENOLS ON BLOOD CHOLESTEROL IN HAMSTERS / Chapter 4.1 --- Introduction --- p.114 / Chapter 4.1.1 --- Apple is a commonly consumed fruit worldwide --- p.114 / Chapter 4.1.2 --- Potential health effects of apples --- p.114 / Chapter 4.1.3 --- Abundance of polyphenols in apple --- p.115 / Chapter 4.1.4 --- Fuji variety of apple --- p.116 / Chapter 4.1.5 --- Objectives --- p.116 / Chapter 4.2 --- Materials and Methods --- p.118 / Chapter 4.2.1 --- Isolation of AP --- p.118 / Chapter 4.2.2 --- Characterization of AP extract --- p.118 / Chapter 4.2.3 --- Effect of AP on CETP activity in vitro --- p.118 / Chapter 4.2.4 --- Effect of AP on blood cholesterol in hamsters --- p.119 / Chapter 4.2.4.1 --- Animals --- p.119 / Chapter 4.2.4.2 --- Diets --- p.120 / Chapter 4.2.4.3 --- Plasma lipids measurement --- p.121 / Chapter 4.2.4.4 --- Plasma CETP activity measurement and immunoreactive mass by Western blotting --- p.123 / Chapter 4.2.4.5 --- "Measurement of liver SREBP-2, LDL-R, HMG-R and CYP7A1 protein abundance by Western blotting" --- p.124 / Chapter 4.2.4.6 --- Statistics --- p.124 / Chapter 4.3 --- Results --- p.125 / Chapter 4.3.1 --- Polyphenol content in AP --- p.125 / Chapter 4.3.2 --- Effect of AP on CETP activity in vitro --- p.125 / Chapter 4.3.3 --- Growth and food intake --- p.128 / Chapter 4.3.4 --- Organ weights --- p.128 / Chapter 4.3.5 --- Effect of AP supplementation on the plasma lipid profile of hamsters --- p.131 / Chapter 4.3.6 --- Effect of AP feeding on plasma CETP activity of the hamsters --- p.131 / Chapter 4.3.7 --- Effect of AP on plasma CETP immunoreactive mass --- p.134 / Chapter 4.3.8 --- Effect of AP on liver SREBP-2 immunoreactive mass --- p.134 / Chapter 4.3.9 --- Effect of AP on liver LDLR immunoreactive mass --- p.134 / Chapter 4.3.10 --- Effect of AP on liver HMGR immunoreactive mass --- p.134 / Chapter 4.3.11 --- Effect of AP on liver CYP7A1 immunoreactive mass --- p.134 / Chapter 4.3.12 --- Effect of AP on liver cholesterol level --- p.140 / Chapter 4.4 --- Discussion --- p.142 / Chapter CHAPTER 5 --- CONCLUSION --- p.145 / REFERENCES --- p.148

Atherosclerosis is a disease of the arteries and is defined as a form of arteriosclerosis in which fatty lesions called atheromatous plaques form on the intima of arteries. The formation of these plaques begins early, within the first two decades of life, and may be started by damage to the endothelial cells and intima of the artery walls (Guyton, 1981). A number of factors may cause the initial damage, including physical abrasion of the endothelium, abnormal substances in the blood or pulsating arterial pressure on the vessel wall (Guyton, 1981). There is a growing body of epidemiologic, genetic, experimental, and clinical evidence to support the hypothesis that there is a cause and effect relationship between high blood levels of cholesterol and the development of atherosclerosis in humans. The purpose of this study was to determine the relationship of exercise and diet in predicting the total cholesterol/high density lipoprotein-cholesterol (TC/HDL-C) ratio in college age males and females. Variables controlled for included age, gender, smoking, medication use, contraceptive use, hormone use and intense physical activity.

Chiu Chi Pang. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 121-134). / Abstracts in English and Chinese. / DECLARATION --- p.i / ACKNOWLEDGEMENTS --- p.ii / ABBREVIATIONS --- p.iii / ABSTRACT --- p.vi / 摘要 --- p.viii / Chapter CHAPTER 1: --- GENERAL INTRODUCTION --- p.1 / Chapter 1.1 --- Cholesterol --- p.1 / Chapter 1.1.1 --- History of cholesterol --- p.1 / Chapter 1.1.2 --- Structure of cholesterol --- p.1 / Chapter 1.1.3 --- Biological function of cholesterol --- p.3 / Chapter 1.1.4 --- Sources of cholesterol in our body --- p.3 / Chapter 1.2 --- Lipid hypothesis --- p.4 / Chapter 1.2.1 --- Relationship between dietary cholesterol and plasma cholesterol --- p.4 / Chapter 1.2.2 --- "Hypercholesterolemia , atherosclerosis and coronary heart disease (CHD)" --- p.4 / Chapter 1.2.3 --- Individual variation --- p.5 / Chapter 1.3 --- Cholesterol homeostasis --- p.7 / Chapter 1.3.1 --- SREBPs up-regulates the expression of LDL-receptor and HMG-CoA reductase --- p.7 / Chapter 1.3.2 --- HMG-CoA reductase as the rate-limiting enzyme in cholesterol synthesis --- p.11 / Chapter 1.3.3 --- LDL-receptor as the major protein removing plasma cholesterol …… --- p.12 / Chapter 1.3.4 --- LXR-α as an activator of CYP7A1 --- p.14 / Chapter 1.3.5 --- CYP7A1 controls the classical pathway for the elimination of hepatic cholesterol --- p.16 / Chapter 1.3.6 --- Bile acids as the metabolites of CYP7A1 --- p.17 / Chapter 1.4 --- Previous works in our laboratory --- p.20 / Chapter 1.5 --- Objective of this project --- p.22 / Chapter CHAPTER 2: --- INCREASED EXPRESSION OF LDL-RECEPTOR IS RESPONSIBLE FOR THE HYPO-RESPONSIVENESS OF RATS TO DIETARY CHOLESTEROL --- p.23 / Chapter 2.1 --- Introduction --- p.23 / Chapter 2.2 --- Objective --- p.24 / Chapter 2.3 --- Methods and materials --- p.25 / Chapter 2.3.1 --- Animals --- p.25 / Chapter 2.3.2 --- Diets --- p.25 / Chapter 2.3.3 --- Determination of serum cholesterol --- p.26 / Chapter 2.3.4 --- Western blot --- p.26 / Chapter 2.3.5 --- Probe production for LDL-receptor --- p.27 / Chapter 2.3.5.1 --- Extraction of total RNA --- p.27 / Chapter 2.3.5.2 --- Reverse-transcription reaction of total RNA --- p.28 / Chapter 2.3.5.3 --- Polymerase chain reaction (PCR) of LDL- receptor fragment from cDNA template --- p.28 / Chapter 2.3.5.4 --- Separation and purification of PCR products --- p.29 / Chapter 2.3.5.5 --- Polishing of purified PCR products --- p.29 / Chapter 2.3.5.6 --- Ligation of PCR products and pPCR-script Amp SK(+) cloning vector --- p.30 / Chapter 2.3.5.7 --- Transformation --- p.30 / Chapter 2.3.5.8 --- Preparing glycerol stocks containing the bacterial clones --- p.31 / Chapter 2.3.5.9 --- Plasmid DNA preparation --- p.31 / Chapter 2.3.5.10 --- Clones confirmation by restriction enzyme digestion --- p.32 / Chapter 2.3.5.11 --- Clones confirmation by automatic sequencing --- p.32 / Chapter 2.3.5.12 --- Linearization of the plasmid DNA --- p.33 / Chapter 2.3.5.13 --- DIG-labeling of RNA probe --- p.35 / Chapter 2.3.5.14 --- Testing of DIG-labeled probe --- p.35 / Chapter 2.3.6 --- Probe production for HMG-CoA reductase --- p.36 / Chapter 2.3.7 --- Probe production for GAPDH --- p.37 / Chapter 2.3.8 --- Northern blot --- p.38 / Chapter 2.3.9 --- Determination of hepatic cholesterol --- p.39 / Chapter 2.3.10 --- Statistics --- p.40 / Chapter 2.4 --- Results --- p.42 / Chapter 2.4.1 --- Growth and food intake --- p.42 / Chapter 2.4.2 --- Effect of cholesterol supplements on serum cholesterol --- p.42 / Chapter 2.4.3 --- Effect of cholesterol supplements on liver cholesterol content --- p.45 / Chapter 2.4.4 --- "Stimulatory effect of high cholesterol diet on nSREBP-2, LDL-receptor and HMG-CoA reductase in rats" --- p.45 / Chapter 2.4.5 --- "Effect of high cholesterol diet on nSREBP-2, LDL-receptor and HMG-CoA reductase in hamsters" --- p.49 / Chapter 2.4.6 --- The regulation of LDL-receptor and HMG-CoA reductase existed at transcriptional level --- p.54 / Chapter 2.5 --- Discussion --- p.59 / Chapter CHAPTER 3: --- RATS ARE HYPO-RESPONSIVE TO DIETARY CHOLESTEROL DUE TO EFFICIENT ELIMINATION OF CHOLESTEROL --- p.67 / Chapter 3.1 --- Introduction --- p.67 / Chapter 3.2 --- Objective --- p.69 / Chapter 3.3 --- Methods and materials --- p.70 / Chapter 3.3.1 --- Animals and diets --- p.70 / Chapter 3.3.2 --- Western blot --- p.70 / Chapter 3.3.3 --- Probe production for CYP7A1 and LXR-α --- p.71 / Chapter 3.3.4 --- Northern blot --- p.71 / Chapter 3.3.5 --- Determination of fecal neutral and acidic sterols --- p.71 / Chapter 3.3.5.1 --- Separation of neutral and acidic sterols --- p.71 / Chapter 3.3.5.2 --- Neutral sterols analysis --- p.72 / Chapter 3.3.5.3 --- Acidic sterols analysis --- p.72 / Chapter 3.3.5.4 --- GLC analysis of neutral and acidic sterols --- p.73 / Chapter 3.3.6 --- Statistics --- p.73 / Chapter 3.4 --- Results --- p.76 / Chapter 3.4.1 --- Effect of cholesterol supplements on fecal total neutral sterols --- p.76 / Chapter 3.4.2 --- Effect of cholesterol supplements on fecal total bile acids --- p.76 / Chapter 3.4.3 --- CYP7A1 protein on rats showed a concentration-dependent increase with response to dietary cholesterol while hamsters did not --- p.79 / Chapter 3.4.4 --- The regulation of CYP7A1 was at transcriptional level --- p.79 / Chapter 3.4.5 --- LXR-α demonstrated a parallel changes in its expression at both translational and transcriptional level --- p.84 / Chapter 3.5 --- Discussion --- p.88 / Chapter CHAPTER 4: --- MECHANISM FOR INDIVIDUAL VARIATION OF SERUM CHOLESTEROL LEVEL IN RATS AND HAMSTERS FED A HIGH CHOLESTEROL DIET --- p.94 / Chapter 4.1 --- Introduction --- p.94 / Chapter 4.2 --- Objective --- p.96 / Chapter 4.3 --- Methods and materials --- p.97 / Chapter 4.3.1 --- Diet and animals --- p.97 / Chapter 4.3.2 --- Western blot --- p.97 / Chapter 4.3.3 --- Statistics --- p.97 / Chapter 4.4 --- Results --- p.99 / Chapter 4.4.1 --- Growth and food intake --- p.99 / Chapter 4.4.2 --- Change of serum cholesterol --- p.99 / Chapter 4.4.3 --- Correlation between various protein expression and serum cholesterol --- p.99 / Chapter 4.4.3.1 --- Correlation between LDL-receptor and serum total cholesterol in rats --- p.99 / Chapter 4.4.3.2 --- Correlation between CYP7A1 and serum total cholesterolin rats --- p.99 / Chapter 4.4.3.3 --- Correlation between nSREBP-2 and serum total cholesterolin rats --- p.105 / Chapter 4.4.3.4 --- Correlation between LXR-a and serum total cholesterol in rats --- p.105 / Chapter 4.4.3.5 --- Correlation between HMG-CoA reductase and serum total cholesterol in rats --- p.105 / Chapter 4.4.3.6 --- Correlation between LDL-receptor and serum total cholesterol in hamsters --- p.105 / Chapter 4.4.3.7 --- Correlation between CYP7A1 and serum total cholesterolin hamsters --- p.109 / Chapter 4.4.3.8 --- Correlation between nSREBP-2 and serum total cholesterolin hamsters --- p.109 / Chapter 4.4.3.9 --- Correlation between HMG-CoA reductase and serum total cholesterol in hamsters --- p.109 / Chapter 4.5 --- Discussion --- p.114 / Chapter CHAPTER 5: --- CONCLUSION --- p.117 / REFERENCES --- p.121

Ma, Ka Ying. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 113-129). / Abstracts in English and Chinese. / ACKNOWLEDGMENTS --- p.I / ABSTRACT --- p.II / LIST OF ABBREVIATIONS --- p.VII / TABLE OF CONTENTS --- p.IX / Chapter Chapter 1 --- General Introduction --- p.1 / Chapter 1.1 --- Calcium --- p.1 / Chapter 1.1.1 --- Recommendation of calcium intake --- p.1 / Chapter 1.1.2 --- Calcium toxicity --- p.2 / Chapter 1.1.3 --- Calcium homeostasis --- p.2 / Chapter 1.1.3.1 --- Role of parathyroid hormone in calcium homeostasis --- p.4 / Chapter 1.1.3.2 --- "Role of 1,25-dihydroxyvitamin D3 in calcium homeostasis" --- p.4 / Chapter 1.1.3.3 --- Role of calcitonin in calcium homeostasis --- p.6 / Chapter 1.2 --- Magnesium --- p.7 / Chapter 1.2.1 --- Recommendation of magnesium intake --- p.7 / Chapter 1.2.2 --- Absorption and secretion of magnesium --- p.8 / Chapter 1.3 --- Cholesterol --- p.9 / Chapter 1.3.1 --- Cholesterol homeostasis --- p.11 / Chapter 1.3.1.1 --- Role of LDLR --- p.14 / Chapter 1.3.1.2 --- Role of SREBP-2 --- p.17 / Chapter 1.3.1.3 --- HMGR as rate limiting step for cholesterol synthesis --- p.19 / Chapter 1.3.1.4 --- CYP7A1 as a key factor in production of bile acids --- p.21 / Chapter 1.3.1.5 --- Role of LXR in production of bile acids --- p.22 / Chapter 1.3.1.6 --- AC AT regulates cholesterol uptake in intestine --- p.22 / Chapter Chapter 2 --- Effect of Calcium Deficiency and Inadequacy on Blood Cholesterol Level in Intact Male and Castrated Hamsters --- p.25 / Chapter 2.1 --- Introduction --- p.25 / Chapter 2.2 --- Objective --- p.28 / Chapter 2.3 --- Materials and methods --- p.29 / Chapter 2.3.1 --- Hamsters --- p.29 / Chapter 2.3.1.1 --- Intact male hamster --- p.29 / Chapter 2.3.1.2 --- Castrated hamster --- p.30 / Chapter 2.3.2 --- Diets --- p.31 / Chapter 2.3.3 --- Determination of calcium content in animal diet --- p.33 / Chapter 2.3.4 --- "Determination of serum lipid, lipoproteins and calcium concentration" --- p.33 / Chapter 2.3.5 --- Determination of cholesterol concentration in organs --- p.34 / Chapter 2.3.6 --- Determination of fecal neutral and acidic sterols --- p.37 / Chapter 2.3.7 --- Determination of fecal neutral sterols --- p.37 / Chapter 2.3.8 --- Determination of fecal acidic sterols --- p.40 / Chapter 2.3.9 --- Statistics --- p.42 / Chapter 2.4 --- Results on intact male hamsters --- p.43 / Chapter 2.4.1 --- Diet composition --- p.43 / Chapter 2.4.2 --- Growth and food intake --- p.43 / Chapter 2.4.3 --- Organ weights --- p.43 / Chapter 2.4.4 --- Effect of calcium deficiency diet on the plasma lipid profile and calcium concentration of hamsters --- p.43 / Chapter 2.4.5 --- Effect of calcium deficiency diet on hepatic cholesterol of hamsters --- p.44 / Chapter 2.4.6 --- Effect of calcium on fecal neutral sterol output --- p.48 / Chapter 2.4.7 --- Effect of calcium on fecal acidic sterol output --- p.48 / Chapter 2.5 --- Results on castrated hamsters --- p.50 / Chapter 2.5.1 --- Growth and food intake --- p.50 / Chapter 2.5.2 --- Organ weights --- p.50 / Chapter 2.5.3 --- Effect of calcium deficiency diet on the plasma lipid profile and calcium concentration of hamsters --- p.50 / Chapter 2.5.4 --- Hepatic cholesterol --- p.50 / Chapter 2.5.5 --- Effect of calcium on fecal neutral sterol output --- p.53 / Chapter 2.5.6 --- Effect of calcium on fecal acidic sterol output --- p.53 / Chapter 2.6 --- Discussion --- p.55 / Chapter Chapter 3 --- Effect of Calcium Deficiency and Inadequacy on Blood Cholesterol Level in Intact Female and Ovariectomized Hamsters --- p.57 / Chapter 3.1 --- Introduction --- p.57 / Chapter 3.2 --- Objective --- p.58 / Chapter 3.3 --- Materials and methods --- p.59 / Chapter 3.3.1 --- Hamsters --- p.59 / Chapter 3.3.1.1 --- Intact female hamster --- p.59 / Chapter 3.3.1.2 --- Ovariectomized hamster --- p.60 / Chapter 3.3.2 --- Diets --- p.60 / Chapter 3.3.3 --- "Determination of serum lipid, lipoproteins and calcium concentration" --- p.60 / Chapter 3.3.4 --- "Determination of cholesterol concentration in organs, fecal neutral and acidic sterols" --- p.60 / Chapter 3.3.5 --- "Western blottting of liver SREBP-2, LDLR, HMGR, LXR and CYP7A1 proteins" --- p.61 / Chapter 3.3.6 --- Preparation of intestinal microsome --- p.62 / Chapter 3.3.7 --- Intestinal acyl coenzyme A: cholesterol acyltransferase (ACAT) activity measurement --- p.63 / Chapter 3.3.8 --- Statistics --- p.64 / Chapter 3.4 --- Results on intact female hamsters --- p.65 / Chapter 3.4.1 --- Growth and food intake --- p.65 / Chapter 3.4.2 --- Organ weights --- p.65 / Chapter 3.4.3 --- Effect of calcium deficiency diet on the plasma lipid profile and calcium concentration of hamsters --- p.65 / Chapter 3.4.4 --- Effect of calcium deficiency diet on hepatic cholesterol of hamsters --- p.65 / Chapter 3.4.5 --- Effect of dietary calcium on fecal neutral sterol output --- p.66 / Chapter 3.4.6 --- Effect of dietary calcium on fecal acidic sterol output --- p.66 / Chapter 3.4.7 --- Effect of dietary calcium on liver LDLR immunoreactive mass --- p.71 / Chapter 3.4.8 --- Effect of dietary calcium on liver CYP7A1 immunoreactive mass --- p.71 / Chapter 3.4.9 --- Effect of dietary calcium on liver LXR immunoreactive mass --- p.71 / Chapter 3.4.10 --- Effect of dietary calcium on liver SREBP-2 immunoreactive mass --- p.71 / Chapter 3.4.11 --- Effect of dietary calcium on liver HMGR immunoreactive mass --- p.71 / Chapter 3.4.12 --- Effect of dietary calcium deficiency on intestinal ACAT activity --- p.77 / Chapter 3.5 --- Results on ovariectomized hamsters --- p.79 / Chapter 3.5.1 --- Growth and food intake --- p.79 / Chapter 3.5.2 --- Organ weights --- p.79 / Chapter 3.5.3 --- Effect of calcium deficiency diet on plasma lipid profile and calcium concentration of hamsters --- p.79 / Chapter 3.5.4 --- Hepatic cholesterol --- p.79 / Chapter 3.5.5 --- Effect of dietary calcium on fecal neutral sterol output --- p.80 / Chapter 3.5.6 --- Effect of dietary calcium on fecal acidic sterol output --- p.80 / Chapter 3.5.7 --- Effect of dietary calcium on liver LDLR immunoreactive mass --- p.85 / Chapter 3.5.8 --- Effect of dietary calcium on liver CYP7A1 immunoreactive mass --- p.85 / Chapter 3.5.9 --- Effect of dietary calcium on liver LXR immunoreactive mass --- p.85 / Chapter 3.5.10 --- Effect of dietary calcium on liver SREBP-2 immunoreactive mass --- p.85 / Chapter 3.5.11 --- Effect of dietary calcium on liver HMGR immunoreactive mass … --- p.85 / Chapter 3.6 --- Discussion --- p.91 / Chapter Chapter 4 --- Effect of Dietary Magnesium Supplementation on Blood Cholesterol Level in Intact Male Hamsters --- p.94 / Chapter 4.1 --- Introduction --- p.94 / Chapter 4.2 --- Objective --- p.96 / Chapter 4.3 --- Materials and methods --- p.97 / Chapter 4.3.1 --- Hamsters --- p.97 / Chapter 4.3.2 --- Diets --- p.98 / Chapter 4.3.3 --- "Determination of serum lipid, lipoproteins and magnesium concentration" --- p.100 / Chapter 4.3.4 --- "Determination of cholesterol concentration in organ, fecal neutral and acidic sterols" --- p.100 / Chapter 4.3.5 --- Statistics --- p.100 / Chapter 4.4 --- Results on male hamster --- p.101 / Chapter 4.4.1 --- Growth and food intake --- p.101 / Chapter 4.4.2 --- Organ weights --- p.101 / Chapter 4.4.3 --- Effect of dietary magnesium on plasma lipid profile and magnesium concentration in hamsters --- p.101 / Chapter 4.4.4 --- Effect of dietary magnesium on hepatic cholesterol of hamsters..… --- p.102 / Chapter 4.4.5 --- Effect of dietary magnesium on fecal neutral sterol output --- p.105 / Chapter 4.4.6 --- Effect of dietary magnesium on fecal acidic sterol output --- p.105 / Chapter 4.6 --- Discussion --- p.107 / Chapter Chapter 5 --- Conclusion --- p.110 / References --- p.113

Cardiovascular disease (CVD) is a major health problem in developed countries and, with increasing prevalence in developing countries and Eastern Europe. Due to the increased incidence with advancing age, there is a need to develop primary preventive interventions to prolong the period of healthy life. Diet has a substantial influence on health and aging. The composition of the human diet plays an important role in the management of lipid and lipoprotein. In this respect, we have focused on the effects of two kinds of functional foods, tea seed oil and dietary onion on their hypocholesterolemic activities and underlying mechanisms in the present study. / Clearly, there are many claims on health benefits of Alliums , however, most, with the exception of garlic, have not received any rigorous or even gentle scientific investigation. Thus, the present study was carried out to explore hypocholesterolemic effects of onion supplementation. After fed for 2 weeks of the high fat high cholesterol diet, thirty-six 8-week male hamsters were divided into four groups. Control group was continued fed with high fat high cholesterol diet, while the other two experimental groups were fed control diet plus 1% (1OP) and 5% (5OP) onion powder for 8 weeks. It was found that feeding high dose of onion powder diet significantly prevented the increase in serum TC, Non-HDL-C and the ratio of non-HDL-C/HDL respectively in hamsters fed a 0.1% cholesterol diet. In contrast, the ratio of HDL/TC in high dose group was significantly increased than that in the control. Low onion dose group tended to have the similar effects as high dose group but, statistically, no difference was observed between the control and low dose groups. Besides, both doses of onion powder diets could significantly countered the increase in serum TG levels. High dose of onion supplementation tended to increase output of fecal neutral and acidic sterols, resulting in reduction of cholesterol retained and absorption. High dose of onion powder diet could significantly up- regulate SREBP-2, LXRbeta, and CYP7A1 protein expressions. The hypocholesterolemic activities of onion might due to the richness in alkyl and alkenyl sulfoxide compounds, anthocyanin, quercetin and cycloalliin, all of which have therapeutic effects. / In conclusion, diet plays an important role in reducing the risk of CVD. This has led to the search for specific foods and food components that may help to improve the serum lipoprotein profile. In present study, tea seed oil and onion was proved to help favorably modify the plasma lipoprotein profile, serving as health supplementation. However, their potential mechanisms were not fully studied and need to be further explored. / Interest in tea seed oil (named tea oil) as a cooking oil is increasing. However, its effect on blood cholesterol is not known. This study was therefore conducted to compare the hypocholesterolemic activity of tea oil with grape seed, canola and corn oils. Fifty 8-week-old male hamsters were first fed a high fat diet (5% lard), and supplemented with 0.1% cholesterol for 2 weeks and then divided into five groups. Control group was continuously fed high fat high cholesterol diet, while the experimental groups were fed high fat, high cholesterol diet plus 10% tea oil, grape seed oil, canola oil and corn oil for 12 weeks. Results showed that plasma total cholesterol (TC), non-HDL-cholesterol (non-HDL-C) and triacylglycerols (TG) in hamsters fed a 0.1% cholesterol diet containing tea, grape, canola or corn oil was significantly reduced compared with those in lard-fed group. Tea oil decreased only non-HDL-C and had no or little effect on HDL-C concentration, while grape oil reduced both. Besides, tea oil-fed hamsters excreted less neutral but greater acidic sterols compared with other three oils. Unlike grape oil, tea oil up-regulated sterol regulatory element binding protein (SREBP-2) and LDL receptor. Differences between tea oil and the tested vegetable oils could be attributable partially to >80% oleic acid in tea oil. / Guan, Lei. / Adviser: Chung Hau Yin. / Source: Dissertation Abstracts International, Volume: 72-04, Section: B, page: . / Thesis (Ph.D.)--Chinese University of Hong Kong, 2010. / Includes bibliographical references (leaves 98-125). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. Ann Arbor, MI : ProQuest Information and Learning Company, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese.