Academic literature on the topic 'Antilipemic agent'

The investigators sought to summarize the percentage reduction in non–high-density lipoprotein cholesterol (non-HDL-C) achieved with various antilipemic regimens and to determine whether certain antilipemic regimens have been proven more effective in lowering non-HDL-C. A search of MEDLINE, International Pharmaceutical Abstracts, and Iowa Drug Information Service Database from 1970 to May 2011 was performed. Criteria were used to exclude studies not published in English, studies with methodology limitations, and studies with variables that may affect efficacy beyond the antilipemic agent administered. Only randomized, controlled trials comparing medications approved by the Food and Drug Administration were reviewed to determine whether significant differences in percentage reduction in non-HDL-C had been observed between different medication regimens. A total of 51 trials reported data that could be used to determine the range of percentage reduction in non-HDL-C achieved by select antilipemic regimens. Of these 51 trials, 38 provided head-to-head comparisons of antilipemic regimens. Rosuvastatin and atorvastatin are the most potent 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) in lowering non-HDL-C. Adding ezetimibe, fibric acid derivatives, and omega-3 fatty acids to antilipemic monotherapy may result in further reduction in non-HDL-C. Subjects with certain characteristics (eg, nonwhite) were not prevalent in these studies.

264W94 was designed to inhibit the ileal bile acid transporter (IBAT). Evaluated in vitro, 264W94 dose-dependently inhibited sodium-dependent uptake of 10 μM [3H]taurocholic acid (TC) by rat and monkey brush border membrane vesicles with IC50s of 0.24 μM and 0.41 μM, and had a competitive profile with Ki of 0.2 μM against TC in Chinese hamster ovary cells expressing human IBAT. In distal ileum in situ, 1–10 μM of 264W94 rapidly decreased uptake of 3mM TC by 24–39%, with corresponding decreases in biliary recovery. In rats and mice in vivo, oral 264W94 decreased absorption of TC analog, 23,25-75Se-homocholic acid taurine (75SeHCAT; quantitated in feces), with ED30 of 0.02 mg/kg bid. 75SeHCAT traced through the GI-tract revealed that peak (97%) inhibition of 75SeHCAT absorption by the distal quarter of small intestine occurred at 4 h after single dose of 264W94 (0.1 mg/kg). Inhibition of IBAT by 264W94 in rats was associated with compensatory, same-day, 4-fold induction of hepatic cholesterol 7α-hydroxylase (CYP7A1) activity, exhibiting normal diurnal fluctuation for 3 days of dosing. In diet induced hypercholesterolemic rats, 264W94 (0.03–1.0 mg/kg bid) dose-dependently reduced serum LDL+VLDL cholesterol up to 61%.In conclusion, 264W94 is a potent new cholesterol lowering agent that acts through inhibition of IBAT and exhibits activity in a human model.

Objective: To examine the prevalence of antilipemic drug use, demographic characteristics of patients using these drugs, and the prevalence of hypercholesterolemia in the Nova Scotia population over 65 years of age. Design: Information was collected on the prescribing of antilipemic drugs using Nova Scotia Medical Services Insurance Pharmacare program data from October 1991 through March 1992. Pharmacare data were compared with prevalence data on increased low-density lipoprotein (LDL) cholesterol concentrations obtained from the Nova Scotia Heart Health Survey (NSHHS). Setting: Pharmacare is a centrally administered drug insurance system maintained in computerized claims files since 1974. It provides prescription drugs to all residents of Nova Scotia who are at least 65 years old and who are insured under the provincial Medicare program. Participants: In the 1991–1992 fiscal year, 47 000 men and 65 700 women were eligible for Pharmacare. The NSHHS was administered to a probability sample of 2108 individuals, representative of the 1986 population aged 18–74 years. Main Outcome Measures: Prescriptions for antilipemic agents. Results: The NSHHS data indicated that 3.7% of women and 2.3% of men at least 65 years old and 4.8% of women and 2.8% of men 65–74 years old received a prescription for antilipemics. Approximately 10% of men and approximately 16% of women aged 65–74 years had LDL cholesterol concentrations in excess of 4.9 mmol/L. Conclusions: Elderly women received antilipemic drugs more frequently than did elderly men. The proportion of Nova Scotia's senior population using antilipemic drugs was less than the proportion with increased serum total cholesterol and LDL cholesterol concentrations. More specific studies need to assess the use of antilipemic drugs in relation to patients' risk factors for cardiovascular disease, patient adherence with antilipemic drug therapy, and the effectiveness of antilipemic drugs.

OBJECTIVE: To determine whether the potentiation of warfarin's anticoagulation effect, which occurred in two patients, was due to an interaction with fenofibrate. CASE SUMMARY: Two patients developed significant potentiation of the anticoagulant effect of warfarin while receiving fenofibrate. In one patient we followed published guidelines to test the potential interaction, including rechallenge twice, and measurements of factors II, V, and VII and liver enzymes to ensure the authenticity of the interaction. We confirmed the interaction by noting that the international normalized ratio (INR) increased with rechallenge, the clotting factor concentrations decreased in concert with the INR, and no other laboratory or clinical factors accounted for this potentiation of the oral anticoagulant affect DISCUSSION: We previously developed criteria specifically for determining the strength of inferred causation in reports of drug interactions with oral anticoagulants; these criteria were adapted from previously described principles of causality assessment. Our observations in two patients suggest a “highly probable” potentiating interaction between fenofibrate and warfarin. Our data do not allow us to draw definitive conclusions on a mechanism of interaction, but fenofibrate is an oral antilipemic agent, similar to clofibrate, that has been described as potentiating oral anticoagulants by affecting coagulation factor synthesis, likely by altering receptor synthesis. Our finding of lower concentrations of coagulation factors suggests a similar mechanism for fenofibrate. Recent data suggest that lipid lowering is effective for primary and secondary prevention of cardiac events. One might therefore expect to see an increase in the use of the various lipid-lowering agents in patients who receive long-term anticoagulation. Our results indicate that the potential for an exaggerated anticoagulant effect occurs within 5–10 days in patients treated with fenofibrate who are receiving long-term anticoagulation with warfarin. CONCLUSIONS: Fenofibrate potentiates the effect of warfarin. Serial monitoring of the INR, at least three times per week, is therefore strongly recommended when initiating fenofibrate therapy in patients receiving warfarin.

Background: Leonurine (Leo), a promising antilipemic agent that has been approved for clinical trials, is extensively metabolized into bioactive Leonurine-10-O-β-glucuronide (L-10-G) vivo. Objective: To explore the effects of breast cancer resistance protein (Bcrp) and multidrug resistance protein 2 (Mrp2) on the disposition of L-10-G. Methods: The pharmacokinetics, tissue distribution and intestinal perfusion of Leo were studied by using efflux transporter gene knockout mouse models. The enzyme kinetics via liver and intestinal microsomes were also examined. Results: After intravenous injection with Leo, the AUC0-∞ values of L-10-G in Bcrp1-/- and Mrp2-/- mice were 1.55-fold and 16.80-fold higher, respectively, than those in wild-type FVB mice (P < 0.05). After oral administration, the AUC0-∞ value of L-10-G showed a 2.82-fold increase in Mrp2-/- mice compared with wild-type FVB mice (P < 0.05). After gavage with Leo for 10 and 25 min, the bile accumulation of L-10-G in Mrp2-/- mice was 3-fold and 22-fold lower, respectively, than that in wild-type FVB mice (P < 0.05). Besides, the intestinal excreted amount of L-10-G showed 2.22-fold and 2.68-fold decrease in Bcrp1-/- and Mrp2-/- mice, respectively, compared with that in wild-type FVB mice (P < 0.05). The clearance of L-10-G decreased in liver microsomes and increased in intestinal microsomes of Bcrp1-/- and Mrp2-/- mice compared to the wild-type FVB mice (P < 0.05). Conclusion: Both Bcrp and Mrp2 are involved in the disposition of L-10-G, and Mrp2 exhibits a superior influence.

Hyperlipidemia is common after renal transplantation. In recent years, much progress has been made in understanding the causes and treatment of lipid abnormalities in renal transplant patients. Recently, short-term studies have shown that newer antilipemic agents appear to be safe and effective in treating hyperlipidemia in this population. Despite the absence of large, controlled clinical trials examining the effect of lipid-lowering strategies on cardiovascular disease and chronic renal allograft rejection, therapy appears to be warranted in renal transplant patients with an atherogenic lipid profile and multiple risk factors.

Abstract Titrating cardiovascular drugs is important to ensure efficacy and to minimize the risk of toxicity. A serum assay is extremely useful to guide digoxin therapy. Assessment of the effect of warfarin on blood clotting should be used to adjust dose. Serum cholesterol and lipid measurements guide therapy with antilipemic agents. The antihypertensive drugs, beta blockers, calcium channel blockers, and vasodilators can be assessed by their clinical effects. There is no strict relation between serum concentration of antiarrhythmic drugs and their effects, nor is it clear that the long-term efficacy of these drugs can be assessed by surrogate end points.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
As dislipidemias têm sido frequentemente encontradas nas crianças e adolescentes devido a obesidade, maus hábitos alimentares e a falta de exercícios físicos. A rosuvastatina atua como inibidor da enzima HMG-CoA redutase e pode ser indicada para a prevenção de doenças cardiovasculares e para o tratamento das dislipidemias, devido a sua grande eficiência na redução das concentrações plasmáticas do colesterol sérico. Este estudo pretendeu investigar o desenvolvimento sexual inicial e os possíveis efeitos reprodutivos adversos na maturidade sexual decorrentes da exposição de ratos juvenis à rosuvastatina na pré-puberdade. Foram formados três grupos aleatoriamente com ratos recém-desmamados (n= 20/por grupo): grupo controle, que recebeu solução salina 0.9%, e os grupos tratados com 3 ou 10 mg/Kg de rosuvastatina por dia via gavagem, desde o dia pós-natal (DPN) 21 até a instalação da puberdade. Parte dos animais de cada grupo (n=10/por grupo) foi eutanasiada no DPN55 e os animais remanescentes foram mantidos até a maturidade sexual e foram eutanasiados no DPN110. No DPN55 foram avaliados as concentrações hormonais, histologia testicular e epididimária e expressão de receptores de andrógenos (AR) no testículo e epidídimo. Na maturidade sexual foram avaliados o comportamento sexual, concentrações hormonais, produção, morfologia e motilidade dos espermatozóides, além da histologia do testículo e epidídimo e imunohistoquímica para AR no testículo. Nos grupos tratados com rosuvastatina, os resultados demonstraram uma tendência para a diminuição das concentrações de testosterona, mas abaixo do nível de significância, bem como houve atraso na idade da instalação da puberdade e no desenvolvimento epididimário. Houve ainda alterações testiculares que podem estar relacionadas com o atraso na puberdade e a diminuição da testosterona. Na maturidade sexual, os animais ...
Dyslipidemias are frequently found in children due to obesity, bad eating habits and the lack of physical exercises. Rosuvastatin acts as an HMG-CoA reductase inhibitor and has been indicated to prevent cardiovascular diseases and to treat dyslipidemias due to its higher efficiency to reduce serum cholesterol concentrations. This study aimed to investigate initial sexual development and the possible reproductive adverse effects on sexual maturity due to juvenile male rats exposure to rosuvastatin during prepuberty. Three groups were formed with newly weaned rats (n= 20/per group): control, whose rats received saline solution 0.9%, rosuvastatin at doses of 3 or 10 mg/Kg daily by gavage, since post-natal day (PND) 21 until puberty onset. Part of each group (n=10/per group) was euthanized on PND55 and the remaining rats (n=10/per group) were maintained until sexual maturity and were euthanized on PND110. On PND55, we analyzed the hormonal concentrations, testicular and epididymal histology and the expression of androgen receptors (AR) on testis and epididymis. During sexual maturity, the parameters evaluated were sexual behavior, hormonal concentrations, sperm production, morphology and motility, besides testicular and epididymal histology and immunohistochemistry for AR. In the rosuvastatin-treated groups, the results demonstrated a trend towards a decrease in testosterone concentration, but below the significance level, as well as delays in both the age of puberty onset and in epididymal development. There were also testicular alterations that might be related to delayed puberty and decrease of serum testosterone. In the adulthood, the rosuvastatin-treated groups showed diminution in follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone concentrations, delay in the latency to the first penis intromission, pathologic alterations on testis and epididymis and decreased sperm ...
FAPESP: 11/15065-5

Orientador: Wilma De Grava Kempinas
Banca: Isabel Cristina Cherici Camargo
Banca: Maria Terezinha Serrão Peraçoli
Resumo: As dislipidemias têm sido frequentemente encontradas nas crianças e adolescentes devido a obesidade, maus hábitos alimentares e a falta de exercícios físicos. A rosuvastatina atua como inibidor da enzima HMG-CoA redutase e pode ser indicada para a prevenção de doenças cardiovasculares e para o tratamento das dislipidemias, devido a sua grande eficiência na redução das concentrações plasmáticas do colesterol sérico. Este estudo pretendeu investigar o desenvolvimento sexual inicial e os possíveis efeitos reprodutivos adversos na maturidade sexual decorrentes da exposição de ratos juvenis à rosuvastatina na pré-puberdade. Foram formados três grupos aleatoriamente com ratos recém-desmamados (n= 20/por grupo): grupo controle, que recebeu solução salina 0.9%, e os grupos tratados com 3 ou 10 mg/Kg de rosuvastatina por dia via gavagem, desde o dia pós-natal (DPN) 21 até a instalação da puberdade. Parte dos animais de cada grupo (n=10/por grupo) foi eutanasiada no DPN55 e os animais remanescentes foram mantidos até a maturidade sexual e foram eutanasiados no DPN110. No DPN55 foram avaliados as concentrações hormonais, histologia testicular e epididimária e expressão de receptores de andrógenos (AR) no testículo e epidídimo. Na maturidade sexual foram avaliados o comportamento sexual, concentrações hormonais, produção, morfologia e motilidade dos espermatozóides, além da histologia do testículo e epidídimo e imunohistoquímica para AR no testículo. Nos grupos tratados com rosuvastatina, os resultados demonstraram uma tendência para a diminuição das concentrações de testosterona, mas abaixo do nível de significância, bem como houve atraso na idade da instalação da puberdade e no desenvolvimento epididimário. Houve ainda alterações testiculares que podem estar relacionadas com o atraso na puberdade e a diminuição da testosterona. Na maturidade sexual, os animais ...
Abstract: Dyslipidemias are frequently found in children due to obesity, bad eating habits and the lack of physical exercises. Rosuvastatin acts as an HMG-CoA reductase inhibitor and has been indicated to prevent cardiovascular diseases and to treat dyslipidemias due to its higher efficiency to reduce serum cholesterol concentrations. This study aimed to investigate initial sexual development and the possible reproductive adverse effects on sexual maturity due to juvenile male rats exposure to rosuvastatin during prepuberty. Three groups were formed with newly weaned rats (n= 20/per group): control, whose rats received saline solution 0.9%, rosuvastatin at doses of 3 or 10 mg/Kg daily by gavage, since post-natal day (PND) 21 until puberty onset. Part of each group (n=10/per group) was euthanized on PND55 and the remaining rats (n=10/per group) were maintained until sexual maturity and were euthanized on PND110. On PND55, we analyzed the hormonal concentrations, testicular and epididymal histology and the expression of androgen receptors (AR) on testis and epididymis. During sexual maturity, the parameters evaluated were sexual behavior, hormonal concentrations, sperm production, morphology and motility, besides testicular and epididymal histology and immunohistochemistry for AR. In the rosuvastatin-treated groups, the results demonstrated a trend towards a decrease in testosterone concentration, but below the significance level, as well as delays in both the age of puberty onset and in epididymal development. There were also testicular alterations that might be related to delayed puberty and decrease of serum testosterone. In the adulthood, the rosuvastatin-treated groups showed diminution in follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone concentrations, delay in the latency to the first penis intromission, pathologic alterations on testis and epididymis and decreased sperm ...
Mestre

Background: Coronary heart disease kills more than 7 million people worldwide each year. High levels of blood fat, cholesterol, contributes significantly to coronary heart disease. Lifestyle changes combined with lipid-lowering drugs, statins, is an effective treatment. But adherence to statins is low, not even a myocardial infarction always contributes to adherence. Adherence requires patient education and good communication between patient and physician. There is no deeper knowledge of why coronary heart patients stops with statin treatment. Objective: To describe how coronary heart patients experience the disease and the statin treatment, and furthermore, opportunities and difficulties to adhere with statin therapy. Design: An exploratory qualitative study. Method: 10 male coronary heart patients, 55-78 years were strategically selected from a cardiology clinic in a larger Swedish hospital. Patients were interviewed individually in a semi-structured form, 2009/2010. Data processing was done according to content analysis and yielded four themes: empowerment, effects, decision basis, and trust. Results: The patients did not mentioned heredity among the factors they could not affect in association with the disease. Several patients saw the medication as a limitation, doubted its efficacy, but mostly took it anyway, at least for a limited time. Medication and illness were associated with each other. Information requirements were in most patients. Many patients wanted to discontinue the statin therapy. Conclusion: Retention of power over the own body, good reference base for decision about adherence, and trust in health care. These are crucial components of patients’ adherence to statin therapy, in connection with coronary heart disease.

Bakgrund: Kranskärlssjukdom dödar drygt 7 miljoner människor i världen per år.

För höga halter av blodfettet kolesterol i blodet bidrar kraftigt till kranskärlssjukdom. Livsstilsförändringar kombinerat med blodfettssänkande läkemedel, statiner, är en effektiv behandling. Följsamheten till statiner är dock låg, inte ens genomgången hjärtinfarkt ökar följsamhet. Följsamhet kräver patientutbildning och god kommunikation mellan patient och läkare. Det saknas djupare kunskap om varför kranskärlspatienter slutar med statiner. Syfte: att beskriva hur kranskärlspatienter upplever sjukdomen och statinbehandlingen, samt möjligheter och svårigheter att följa statinbehandlingen. Design: explorativ kvalitativ studie. Metod: 10 manliga kranskärlspatienter, 55-78 år valdes strategiskt via en kardiologklinik på ett större svenskt sjukhus. Patienterna intervjuades personligen i semistrukturerad form, 2009/2010. Databearbetning skedde enligt innehållsanalys och gav fyra teman: egenmakt, effekter, beslutsgrund, tilltro. Resultat: Patienterna nämnde inte ärftlighet bland faktorer som ansågs opåverkbara i samband med kranskärlssjukdomen. Flera patienter såg medicinen som en begränsning och tvivlade på effekten, men tog den oftast ändå, åtminstone under en begränsad tid. Likhetstecken sattes mellan medicinering och sjukdom. Informationsbehov fanns hos flertalet patienter. Många patienter ville sluta med statinbehandlingen. Slutsats: Bibehållen makt över sin egen kropp, god referensgrund för beslut om följsamhet samt förtroende för sjukvården, är avgörande förutsättningar för kranskärlspatienters följsamhet till statinbehandling.

Yeung Ming.
Thesis (M.Phil.)--Chinese University of Hong Kong, 2003.
Includes bibliographical references (leaves 136-162).
Abstracts in English and Chinese.
THESIS COMMITTEE --- p.i
ACKNOWLEDGEMENTS --- p.ii
ABSTRACT (ENGLISH) --- p.iii~v
ABSTRACT (CHINESE) --- p.vi~vii
TABLE OF CONTENTS --- p.viii~xiii
LIST OF TABLES --- p.xiv~xv
LIST OF FIGURES --- p.xvi~xviii
LIST OF ABBREVIATIONS --- p.xix~xx
Chapter CHAPTER ONE: --- INTRODUCTION --- p.1
Chapter 1.1 --- Different lipoproteins and their functions --- p.1
Chapter 1.1.1 --- Chylomicrons --- p.4
Chapter 1.1.2 --- VLDL --- p.4
Chapter 1.1.3 --- LDL --- p.4
Chapter 1.1.4 --- HDL --- p.5
Chapter 1.2 --- Risk factors of coronary heart disease (CHD) --- p.5
Chapter 1.2.1 --- Background information of CHD --- p.6
Chapter 1.2.2 --- "Relationship between serum total cholesterol (TC), Low-density lipoprotein (LDL) cholesterol and CHD" --- p.7
Chapter 1.2.3 --- High-density lipoprotein (HDL) cholesterol and CHD --- p.8
Chapter 1.2.4 --- Triglyceride and CHD --- p.9
Chapter 1.3 --- Cholesterol homeostasis --- p.10
Chapter 1.3.1 --- Roles of HMG-CoA reductase in cholesterol biosynthesis --- p.13
Chapter 1.3.2 --- Roles of cholesterol 7α-hydroxylase (CYP7A) in cholesterol catabolism…… --- p.15
Chapter 1.3.3 --- Effects of Short-Chain Fatty Acid (SCFA) --- p.17
Chapter 1.3.4 --- Related hormone --- p.18
Chapter 1.4 --- Possible mechanisms of hypolipidemic agents --- p.19
Chapter 1.4.1 --- Hypolipidemic functional foods --- p.20
Chapter 1.4.2 --- Pharmacological drugs --- p.26
Chapter 1.5 --- Edible and medicinal mushrooms --- p.28
Chapter 1.5.1 --- General introduction --- p.28
Chapter 1.5.2 --- Hypolipidemic agents from Fungi --- p.31
Chapter 1.6 --- Animal model --- p.35
Chapter 1.7 --- Objectives --- p.36
Chapter CHAPTER TWO: --- MATERIALS AND METHODS --- p.37
Chapter 2.1 --- Materials --- p.37
Chapter 2.1.1 --- Mushroom samples and control --- p.37
Chapter 2.1.1.1 --- Sample introduction --- p.37
Chapter 2.1.1.2 --- Sample collection --- p.40
Chapter 2.1.1.3 --- Sample preparation --- p.41
Chapter 2.1.1.4 --- Moisture content --- p.45
Chapter 2.1.2 --- Animal diets for different experiments --- p.45
Chapter 2.1.2.1 --- Basal diet --- p.45
Chapter 2.1.2.2 --- Diet for preliminary screening --- p.46
Chapter 2.1.2.3 --- Diet for dosage experiment --- p.46
Chapter 2.1.2.4 --- Diet for active ingredient experiments --- p.47
Chapter 2.1.2.5 --- Diet for long-term feeding experiment --- p.47
Chapter 2.1.3 --- Animal model --- p.49
Chapter 2.2 --- Methods --- p.49
Chapter 2.2.1 --- Nutritional components of mushroom samples --- p.49
Chapter 2.2.1.1 --- Crude protein content (Kjeldahl method) --- p.49
Chapter 2.2.1.2 --- Total dietary fiber content --- p.50
Chapter 2.2.1.3 --- Crude lipid content --- p.52
Chapter 2.2.1.4 --- Ash content --- p.53
Chapter 2.2.1.5 --- Moisture content --- p.53
Chapter 2.2.2 --- Animal handling experiments --- p.54
Chapter 2.2.2.1 --- Feeding experiment standards --- p.54
Chapter 2.2.2.1.1 --- Feeding experiments of preliminary screening test --- p.54
Chapter 2.2.2.1.2 --- Feeding experiments of dosage test --- p.55
Chapter 2.2.2.1.3 --- Feeding experiments of solvent extracts from Agrocybe aegerita (Brig) Sing (AA) --- p.56
Chapter 2.2.2.1.3.1 --- Fractionation of ethanol & water soluble components of AA --- p.56
Chapter 2.2.2.1.3.2 --- Feeding experiments of ethanol & water soluble components of AA --- p.57
Chapter 2.2.2.1.4 --- Feeding experiment of long-term test --- p.58
Chapter 2.2.2.2 --- Blood sample collection --- p.58
Chapter 2.2.2.3 --- Serum preparation --- p.58
Chapter 2.2.2.4 --- Liver sample preparation --- p.58
Chapter 2.2.2.5 --- Fecal sample preparation --- p.59
Chapter 2.2.3 --- Determination of serum lipid profiles --- p.59
Chapter 2.2.3.1 --- Serum total cholesterol (TC) assay --- p.59
Chapter 2.2.3.2 --- Serum triglyceride (TG) assay --- p.60
Chapter 2.2.3.3 --- Serum high-density lipoprotein (HDL) cholesterol assay --- p.61
Chapter 2.2.3.3.1 --- Separation of HDL fraction --- p.61
Chapter 2.2.3.3.2 --- HDL cholesterol (HDL-c) determination --- p.61
Chapter 2.2.4 --- Determination of liver lipid profiles --- p.62
Chapter 2.2.4.1 --- Liver total cholesterol (TC) level determination --- p.62
Chapter 2.2.4.2 --- Determination of liver total lipid (TL) level --- p.64
Chapter 2.2.5 --- Quantitative determination of fecal neutral & acidic sterols --- p.64
Chapter 2.2.5.1 --- Separation of fecal neutral & acidic sterols --- p.64
Chapter 2.2.5.2 --- Derivatisation of fecal neutral sterols --- p.65
Chapter 2.2.5.3 --- Derivatisation of fecal acidic sterols --- p.65
Chapter 2.2.5.4 --- Gas chromatographic analysis of fecal neutral & acidic sterols --- p.66
Chapter 2.2.6 --- Assays of liver key enzymes in cholesterol metabolism --- p.67
Chapter 2.2.6.1 --- Preparation of hepatic microsome --- p.67
Chapter 2.2.6.2 --- Assay of HMG-CoA reductase activity --- p.68
Chapter 2.2.6.3 --- Assay of CYP7A activity --- p.69
Chapter 2.3 --- Data statistics --- p.71
Chapter CHAPTER THREE: --- RESULTS AND DISCUSSION --- p.72
Chapter 3.1 --- Preliminary screening of eleven mushrooms for their hypolipidemic effect in hyperlipidemic S.D. rats --- p.72
Chapter 3.1.1 --- Body weight and food intake --- p.73
Chapter 3.1.2 --- Effect of mushroom supplementation on serum lipid profiles --- p.75
Chapter 3.1.2.1. --- Effect of mushroom supplementation on serum TC levels --- p.75
Chapter 3.1.2.2. --- Effect of mushroom supplementation on serum TG levels --- p.77
Chapter 3.1.2.3. --- Effect of mushroom supplementation on serum HDL levels --- p.79
Chapter 3.1.2.4 --- Discussion of serum lipid profiles of S.D. rats fed M.S. diets in mushroom screening experiments --- p.83
Chapter 3.1.3 --- Effect and discussion of mushroom supplementation on hepatic lipid profiles --- p.84
Chapter 3.1.4 --- Effect and discussion of mushroom supplementation on fecal neutral sterol excretion --- p.87
Chapter 3.1.5 --- Summary (mushroom screening experiments) --- p.90
Chapter 3.2 --- Hypolipidemic effect of Agrocybe aegerita (Brig.) Sing (AA) in a dose response study in hyperlipidemic S.D. rats --- p.91
Chapter 3.2.1 --- Nutritional composition of AA mushroom --- p.91
Chapter 3.2.2 --- Body weight and food intake --- p.91
Chapter 3.2.3 --- Effect of three different dosages of AA mushroom supplementation on blood lipid profiles of S.D. rats --- p.93
Chapter 3.2.3.1 --- Effect of different dosages of AA mushroom supplementation diets on serum TC level --- p.93
Chapter 3.2.3.2 --- Effect of different dosages of AA mushroom supplementation diets on serum TG level --- p.93
Chapter 3.2.3.3 --- Effect of different dosages of AA mushroom supplementation diets on serum HDL level --- p.95
Chapter 3.2.3.4 --- Discussion of different dosages of AA mushroom supplementation diets on serum lipid profiles --- p.97
Chapter 3.2.4 --- Effect and discussion of three different dosages of AA mushroom supplementation on hepatic lipid profiles --- p.98
Chapter 3.2.5 --- Effect and discussion of three different dosages of AA mushroom supplementation on fecal neutral & acidic sterol excretion --- p.101
Chapter 3.2.6 --- Summary (dose response study) --- p.105
Chapter 3.3 --- Hypolipidemic effect of ethanol extract (E.E.) & water extract (W.E.) from AA in hyperlipidemic S.D. rats --- p.106
Chapter 3.3.1 --- Extraction yield --- p.106
Chapter 3.3.2 --- Body weight & food intake --- p.106
Chapter 3.3.3 --- Effect of AA extract supplementation on serum lipid profiles --- p.107
Chapter 3.3.3.1 --- Effect of AA extract supplementation on serum TC level --- p.107
Chapter 3.3.3.2 --- Effect of AA extract supplementation on serum TG level --- p.108
Chapter 3.3.3.3 --- Effect of AA extract supplementation on serum HDL level --- p.109
Chapter 3.3.4 --- Effect of AA extract supplementation on hepatic lipid profiles --- p.111
Chapter 3.3.5 --- Effect of AA extract supplementation on fecal neutral & acidic sterols excretion --- p.111
Chapter 3.3.6 --- Discussion (active fraction extract study) --- p.113
Chapter 3.4 --- Long-term evaluation of the hypolipidemic effect of AA supplementation in normolipic S.D. rats --- p.116
Chapter 3.4.1 --- Body weight & food intake --- p.116
Chapter 3.4.2 --- Effect of long term AA supplementation on serum lipid profiles --- p.117
Chapter 3.4.2.1 --- Effect of long term AA supplementation on serum TC level --- p.117
Chapter 3.4.2.2 --- Effect of long term AA supplementation on serum TG level --- p.118
Chapter 3.4.2.3 --- Effect of long term AA supplementation on serum HDL level --- p.119
Chapter 3.4.3 --- Effect of long term AA supplementation on hepatic lipid profiles --- p.119
Chapter 3.4.4 --- Effect of long term AA supplementation on fecal neutral & acidic sterols excretion --- p.121
Chapter 3.4.5 --- Effect of long term AA supplementation on hepatic key enzymes of cholesterol metabolism ´ؤ HMG-CoA reductase and CYP7A --- p.123
Chapter 3.4.5.1 --- Quantitation of hepatic microsomal protein --- p.123
Chapter 3.4.5.2 --- Effect of long term AA supplementation on HMG-CoA reductase activity in S.D. rats --- p.124
Chapter 3.4.5.3 --- Effect of long term AA supplementation on CYP7A activity in S.D. rats --- p.124
Chapter 3.4.7 --- Discussion (long-term study) --- p.126
Chapter CHAPTER FOUR: --- CONCLUSION AND FUTURE PERSPECTIVES --- p.130
References --- p.136

by Chan Ping Tim Timothy.
Thesis (M.Phil.)--Chinese University of Hong Kong, 1997.
Includes bibliographical references (leaves 129-141).
ACKNOWLEDGMENTS --- p.I
ABSTRACT --- p.II
LIST OF ABBREVIATIONS --- p.IV
TABLE OF CONTENTS --- p.VI
Chapter CHAPTER 1 --- GENERAL INTRODUCTION --- p.1
Chapter 1.1 --- History of tea --- p.1
Chapter 1.2 --- Botany and agriculture of tea --- p.1
Chapter 1.3 --- Classification of tea --- p.2
Chapter 1.4 --- Composition of tea --- p.4
Chapter 1.5 --- Tea processing --- p.8
Chapter 1.5.1 --- Manufacture of green tea --- p.8
Chapter 1.5.2 --- Manufacture of black tea --- p.8
Chapter 1.5.3 --- Manufacture of oolong tea --- p.10
Chapter 1.6 --- Pharmacological effects of tea catechins --- p.13
Chapter 1.6.1 --- Antioxidative activity --- p.13
Chapter 1.6.2 --- Hypolipidemic activity --- p.14
Chapter 1.6.3 --- Antimutagenic activity --- p.15
Chapter 1.6.4 --- Anticarcinogenic activity --- p.15
Chapter 1.6.5 --- Antibacterial activity --- p.16
Chapter CHAPTER 2 --- ANTIOXIDATIVE ACTIVITIES OF TEA ETHANOL EXTRACTS AND GTC ON OXIDATION OF CANOLA OIL --- p.18
Chapter 2.1 --- Introduction --- p.18
Chapter 2.1.1 --- Lipid oxidation in food --- p.18
Chapter 2.1.2 --- Phenolic antioxidants --- p.19
Chapter 2.1.2.1 --- Major phenolic antioxidants used in food --- p.19
Chapter 2.1.2.2 --- Mechanism of action of phenolic antioxidants --- p.20
Chapter 2.1.2.3 --- BHA and its safety --- p.22
Chapter 2.1.2.4 --- BHT and its safety --- p.24
Chapter 2.1.3 --- Natural antioxidants --- p.24
Chapter 2.2 --- Objectives --- p.26
Chapter 2.3 --- Materials --- p.28
Chapter 2.4 --- Methods --- p.28
Chapter 2.4.1 --- GTC extraction --- p.28
Chapter 2.4.2 --- "HPLC analysis of GTC," --- p.29
Chapter 2.4.3 --- Isolation and purification of individual epicatechin isomers --- p.30
Chapter 2.4.4 --- Ethanol extraction of tea --- p.30
Chapter 2.4.5 --- Effect of tea ethanol extracts on oxygen consumption of canola --- p.31
Chapter 2.4.6 --- Effect of GTC on oxygen consumption of canola oil --- p.32
Chapter 2.4.7 --- Fatty acid analysis --- p.32
Chapter 2.4.8 --- Thermal loss of BHT --- p.33
Chapter 2.4.9 --- Thermal loss of GTC --- p.33
Chapter 2.4.10 --- Statistics --- p.35
Chapter 2.5 --- Results --- p.37
Chapter 2.5.1 --- Antioxidative activities of tea ethanol extracts --- p.37
Chapter 2.5.2 --- The yield and composition of GTC from jasmine tea --- p.51
Chapter 2.5.3 --- Antioxidative activity of GTC --- p.55
Chapter 2.5.4 --- Antioxidative activities of individual epicatechin isomers --- p.55
Chapter 2.5.5 --- Thermal loss of GTC --- p.60
Chapter 2.6 --- Discussion --- p.62
Chapter 2.6.1 --- Contribution of catechins to the antioxidative effects of tea ethanol extracts --- p.62
Chapter 2.6.2 --- Antioxidaitve activities of different types of teas --- p.62
Chapter 2.6.3 --- Proposed mechanisms for the relative activity of epicatechin isomers --- p.63
Chapter 2.6.4 --- Loss of BHT via volatilization --- p.66
Chapter 2.6.5 --- Potential of tea catechins as food antioxidants --- p.67
Chapter 2.6.5.1 --- Safety of GTC --- p.67
Chapter 2.6.5.2 --- Solubility of GTC --- p.68
Chapter 2.6.5.3 --- Effects of GTC on food quality --- p.68
Chapter CHAPTER 3 --- INHIBITORY EFFECTS OF GTC AND EPICATECHIN ISOMERS ON IN VITRO CU2+-MEDIATED LDL OXIDATION --- p.70
Chapter 3.1 --- Introduction --- p.70
Chapter 3.1.1 --- Mechanisms of LDL oxidation --- p.71
Chapter 3.1.1.1 --- Nature and sources of oxidants underlying LDL oxidation --- p.71
Chapter 3.1.1.2 --- Structural changes of ox-LDL --- p.72
Chapter 3.1.2 --- Biological effects of ox-LDL --- p.74
Chapter 3.1.3 --- Antioxidants and atherosclerosis --- p.76
Chapter 3.2 --- Objectives --- p.78
Chapter 3.3 --- Materials and methods --- p.79
Chapter 3.3.1 --- LDL isolation --- p.79
Chapter 3.3.2 --- LDL oxidation --- p.79
Chapter 3.3.3 --- Thiobarbituric acid-reactive substance (TBARS) assay --- p.80
Chapter 3.3.4 --- Lipid analysis --- p.80
Chapter 3.3.5 --- Statistics --- p.81
Chapter 3.4 --- Results --- p.82
Chapter 3.4.1 --- Protective effects of GTC against LDL oxidation --- p.82
Chapter 3.4.2 --- Varying protective effects of individual epicatechin isomers --- p.82
Chapter 3.4.3 --- Protective effects of GTC against oxidative degradation of PUFAs in LDL --- p.86
Chapter 3.5 --- Discussion --- p.88
Chapter 3.5.1 --- Tea catechins as anti-atherogenic agents --- p.88
Chapter 3.5.2 --- Mechanisms of the protective effects of tea catechins against Cu2+-induced LDL oxidation --- p.88
Chapter 3.5.3 --- Relative antioxidative activities of epicatchin isomers --- p.89
Chapter 3.5.4 --- Absorption of tea catechins --- p.90
Chapter 3.5.5 --- Pro-oxidant activities of tea catechins --- p.91
Chapter CHAPTER 4 --- HYPOLIPIDEMIC ACTIVITY OF GTC --- p.93
Chapter 4.1 --- Introduction --- p.93
Chapter 4.1.1 --- High serum cholesterol as a risk factor of CHD --- p.93
Chapter 4.1.2 --- Serum TG and CHD --- p.94
Chapter 4.1.3 --- Hypolipidemic effect of tea --- p.95
Chapter 4.1.4 --- Hamster as an animal model of cholesterol metabolism --- p.96
Chapter 4.2 --- Objectives --- p.97
Chapter 4.3 --- Materials and methods --- p.98
Chapter 4.3.1 --- Animals --- p.98
Chapter 4.3.2 --- Experiment 1 --- p.98
Chapter 4.3.3 --- Experiment 2 --- p.100
Chapter 4.3.4 --- Experiment 3 --- p.101
Chapter 4.3.5 --- "Serum lipid, lipoprotein and apolipoprotein determinations" --- p.101
Chapter 4.3.6 --- Lipid analysis of liver and carcass --- p.102
Chapter 4.3.7 --- Analysis of fecal lipid content --- p.102
Chapter 4.3.8 --- Determination of hepatic cholesterol content --- p.103
Chapter 4.3.9 --- Assay of fatty acid synthase activity --- p.105
Chapter 4.3.10 --- Statistics --- p.105
Chapter 4.4 --- Results --- p.106
Chapter 4.4.1 --- Growth and food intake --- p.106
Chapter 4.4.2 --- Effects of different levels of dietary GTC on serum TG and cholesterol --- p.106
Chapter 4.4.3 --- Time course study of the hypolipidemic effects of dietary GTC --- p.109
Chapter 4.4.4 --- Effects of GTWE on serum lipid and apolipoprotein profiles --- p.113
Chapter 4.4.5 --- "Effects of dietary GTC on hepatic TG, FFA and cholesterol contents" --- p.113
Chapter 4.4.6 --- "Effects of dietary GTC on carcass TG, FFA and cholesterol contents" --- p.118
Chapter 4.4.7 --- Effects of dietary GTC on fatty acid synthase activity --- p.118
Chapter 4.4.8 --- Effects of dietary GTC on fecal lipids content --- p.118
Chapter 4.5 --- Discussion --- p.120
Chapter 4.5.1 --- Hypolipidemic effect of GTC --- p.120
Chapter 4.5.2 --- Effects of GTC on serum apolipoproteins --- p.120
Chapter 4.5.3 --- Implication of GTC intake in humans --- p.121
Chapter 4.5.4 --- Mechanisms for the hypolipidemic activity of GTC --- p.122
Chapter 4.5.5 --- Reduction in hepatic TG and FFA contents in GTC-fed hamsters --- p.123
Chapter 4.5.6 --- Suppression of body lipid accumulation by dietary GTC --- p.124
Chapter 4.5.7 --- Mechanisms for the hypocholesterolemic activity of GTC --- p.124
Chapter CHAPTER 5 --- CONCLUSIONS --- p.126
REFERENCES --- p.129