No abstract available.
Cholesterol ; Cholesterol, LDL ; Humans ; Lipoproteins

This study was performed to examine the combined effects of gamma linolenic acid and isoflavone supplementation on menopausal symptoms and serum lipids in 73 postmenopausal women. A total subjects were randomly assigned to isoflavone (30 mg) + gamma-linolenic acid (110 mg) group or placebo group. We measured menopausal symptoms by modified Kupperman Index (KI) and oxidized LDL, lipid peroxides, blood components and anthropometric parameters before and after the 12 week intervention period. After the 12 weeks of supplementation, supplement group and placebo group showed a significant reduction of modified kupperman index (p < 0.001). Isoflavone (30 mg) + gamma-linolenic acid (110 mg) supplement group showed a significant reduction of oxidized LDL cholesterol concentration (p = 0.006) whereas placebo group did not show significant change. Isoflavone and gamma-linolenic acid consumption did not significantly affect plasma concentrations of total, LDL, HDL cholesterol, triglyceride, apo A1, B and blood components. The result of present study demonstrated the supplementation of 30 mg isoflavone and 110 mg gamma-linolenic acid per day for 12 weeks may protect LDL cholesterol from oxidative stress.
Apolipoprotein A-I ; Cholesterol, HDL ; Cholesterol, LDL ; Female ; gamma-Linolenic Acid ; Humans ; Lipid Peroxides ; Lipoproteins, LDL ; Oxidative Stress ; Plasma

Both metabolic syndrome (MetS) and elevated LDL cholesterol (LDL-C) increase the risk for cardiovascular disease (CVD). We hypothesized that low HDL cholesterol (HDL-C) would further increase CVD risk in women having both conditions. To assess this, we recruited 89 women with MetS (25-72 y) and LDL-C > or = 2.6 mmol/L. To determine whether plasma HDL-C concentrations were associated with dietary components, circulating atherogenic particles, and other risk factors for CVD, we divided the subjects into two groups: high HDL-C (H-HDL) (> or = 1.3 mmol/L, n = 32) and low HDL-C (L-HDL) (< 1.3 mmol/L, n = 57). Plasma lipids, insulin, adiponectin, apolipoproteins, oxidized LDL, Lipoprotein(a), and lipoprotein size and subfractions were measured, and 3-d dietary records were used to assess macronutrient intake. Women with L-HDL had higher sugar intake and glycemic load (P < 0.05), higher plasma insulin (P < 0.01), lower adiponectin (P < 0.05), and higher numbers of atherogenic lipoproteins such as large VLDL (P < 0.01) and small LDL (P < 0.001) than the H-HDL group. Women with L-HDL also had larger VLDL and both smaller LDL and HDL particle diameters (P < 0.001). HDL-C was positively correlated with LDL size (r = 0.691, P < 0.0001) and HDL size (r = 0.606, P < 0.001), and inversely correlated with VLDL size (r = -0.327, P < 0.01). We concluded that L-HDL could be used as a marker for increased numbers of circulating atherogenic lipoproteins as well as increased insulin resistance in women who are already at risk for CVD.
Adiponectin ; Apolipoproteins ; Cardiovascular Diseases ; Cholesterol, HDL ; Cholesterol, LDL ; Diet Records ; Female ; Humans ; Insulin ; Insulin Resistance ; Lipoprotein(a) ; Lipoproteins ; Lipoproteins, LDL ; Plasma ; Risk Factors

Lipoprotein lipase (LPL) is known to be attached to the luminal surface of vascular endothelial cells in a complex with membrane-bound heparan sulfate, and released into blood stream by heparin. LPL that catalyzes hydrolysis of triglyceride (TGL) on chylomicron and VLDL into two fatty acids and monoacylglycerol, is also implicated to participate in an enhancement of cholesterol uptake by arterial endothelial cells in vitro. But little is known about the LPL-mediated cholesterol uptake in physiological state. In this study, changes in blood lipid composition and levels of lipoproteins were determined after the injection of heparin in human. The level of LPL in plasma was increased from 0 to 11 mU/ml within 30-40 min post-heparin administration and decreased to the basal level within 2 h. The level of TGL in plasma decreased from 70 mg/dl to 20 mg/dl within 1 h and gradually increased to 80 mg/dl within 4 h. However the level of total cholesterol in plasma remained at 140 mg/dl during an experimental period of 4 h. Analysis of Lipoproteins in plasma by NaBr density gradient ultracentrifugation showed that the level of VLDL decreased from 50 mg/dl to 10 mg/dl within 1-2 h and returned to normal plasm level at 4 h. However there were no significant changes in the level of LDL and HDL. These results suggest that, at least, in normo-lipidemic subjects, increased free plasm LPL acts primarily on VLDL and failed to show any significant uptake of cholesterol-rich lipoproteins in human.
Adult ; Cholesterol/blood ; Heparin/pharmacology* ; Heparin/administration & dosage ; Human ; Immunoblotting ; Lipoprotein Lipase/blood* ; Lipoproteins/blood* ; Lipoproteins, HDL/blood ; Lipoproteins, LDL/blood ; Lipoproteins, VLDL/blood ; Triglycerides/blood

Despite the excellent success of lowering low-density lipoprotein cholesterol (LDLc) cholesterol for treating coronary heart disease (CHD), a major part of the population still suffer from CHD. This fact is more prominent among the high risk patients who receive lipid lowering treatment with statins. This treatment is based on the prevailing view that LDL cholesterol (LDLc) is the only important risk factor for CHD. It is well known that HDL plays a crucial role for preventing CHD. Several epidemiologic studies and clinical trials have reported that high density lipoprotein cholesterol (HDLc) is an independent risk factor for CHD as well. A large scale meta-analysis of clinical trials clearly supports that increasing HDLc is equally important as decreasing LDLc, suggesting that physicians should pay attention to increasing HDLc as well as decreasing LDLc. Ongoing trials that are focused on this issue will test this hypothesis in the near future.
Cholesterol ; Cholesterol, HDL* ; Cholesterol, LDL ; Coronary Disease ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoproteins ; Risk Factors

BACKGROUND: Dyslipidemia is a disorder of lipid metabolism, including elevated total cholesterol, elevated triglyceride, elevated low density lipoprotein cholesterol (LDL-C), and decreased high density lipoprotein cholesterol (HDL-C). The objective of this study was to investigate recent changes in the prevalence of dyslipidemia and also the rates of awareness, treatment, and control of dyslipidemia among Korean adults. METHODS: Dyslipidemia is defined according to the National Cholesterol Education Program-Adult Treatment Panel III as total cholesterol > or =240 mg/dL, LDL-C > or =160 mg/dL, HDL-C <40 mg/dL, and triglyceride > or =200 mg/dL. The prevalence of dyslipidemia was estimated for adults aged > or =20 years using the Korea National Health and Nutrition Survey (KNHANES) in 1998 (n=6,923), 2001 (n=4,882), and 2005 (n=5,323). Rates of awareness, treatment and control of dyslipidemia were calculated for adults aged > or =30 years using the KNHANES in 2005 (n=4,654). RESULTS: The prevalence of dyslipidemia (aged > or =20 years) increased from 32.4% in 1998 to 42.6% in 2001 and 44.1% in 2005. Compared with the KNHANES in 1998, the prevalence of dyslipidemia was 47% (95% confidence interval [CI], 35% to 59%) higher in 2001 and 61% (95% CI, 49% to 75%) higher in 2005. In 2005, only 9.5% of people with dyslipidemia were aware of the disease, 5.2% used lipid-lowering medication, and 33.2% of patients with treatment reached treatment goals. CONCLUSION: The prevalence of dyslipidemia in Korea gradually increased between 1998 and 2005. These findings suggest that more intense efforts for the prevention and treatment of dyslipidemia may lead to further improvement in the management of dyslipidemia.
Adult ; Aged ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Dyslipidemias ; Humans ; Korea ; Lipid Metabolism ; Lipoproteins ; Nutrition Surveys ; Prevalence

A new hypolipidemic agent, lovastatin, hydroxy-methyl-gultaryl coenzyme A reductase inhibitor was administred to 25 patients with primary hyperlipidemia 20 to 40 mg daily for 12 weeks and sequential changes of serum lipid profile were analysed as follow. 1) Mean average at baseline period of serum total cholesterol, triglyceride, HDL and low desity lipoprotein cholesterol were 271, 179, 51 and 185 mg/dl respectively. 2) Total cholesterol showed 20% decrease at 4th week and 23% decrease at the end of 12th week while low density lipoprotein cholesterol decreased 31% and 33% respectively. 3) Triglyceride dropped 7% at 8th week and 3% at 12th week. High density lipoprotein cholesterol increased 4% at 4th week and showed 2% decrease at the end of study. 4) Only one patient complained of moderate abdominal pain, which subsided after 2 weeks drug withdrawal. In conclusion, lovastatin was well tolerated and effective, in the treatment of primary hyperlipidemia.
Abdominal Pain ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Coenzyme A ; Humans ; Hyperlipidemias* ; Lipoproteins ; Lovastatin ; Oxidoreductases ; Triglycerides

Serum lipids and lipoproteins were determined in 70 patients with hypertension, 40 patients with cerebral infarctions, and 41 patients with cerebral hemorrhage. The results were compared with findings in 64 healthy controls. The results are as follows; 1) Total cholesterol, VLDL-cholesterol, LDL cholesterol and total cholesterol/HDL-cholesterol ratio were significantly higher in patients with hypertension or cerebral infarction than in control group, but HDL-cholesterol showed no significant difference. 2) In Patients with cerebral hemorrhage, total cholesterol, LDL-cholesterol and HDL-cholesterol were higher than in normal controls. Total cholesterol/HDL-cholesterol ratio was within the limits of normal. It is possible that the susceptibility to cerebral infarction is the result of high total cholesterol/HDL cholesterol ratio rather than low HDL cholesterol. But our study suggests that hyperlipoproteinemia plays a minor role in the development of cerebral hemorrhage.
Cerebral Hemorrhage ; Cerebral Infarction ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Humans ; Hyperlipoproteinemias ; Hypertension* ; Lipoproteins

Animals ; Arteriosclerosis ; drug therapy ; Cholesterol, LDL ; blood ; Drugs, Chinese Herbal ; pharmacology ; Hyperlipidemias ; drug therapy ; Lipids ; blood ; Lipoproteins ; blood ; Lipoproteins, LDL ; blood ; Male ; Rabbits ; Tablets ; Triglycerides ; blood

BACKGROUND/AIMS: Lowering low-density lipoprotein cholesterol (LDL-C) is the primary target for the prevention of cardiovascular disease. Previous studies have shown that estimated LDL-C levels calculated using Friedewald's formula (FLDL-C) are closely correlated with directly measured LDL-C levels (DLDL-C). However, because statins not only reduce LDL-C, but also alter the levels of parameters used to calculate FLDL-C (i.e., total cholesterol, triglycerides, and high-density lipoprotein cholesterol), whether calculated LDL-C levels remain a reliable estimate of actual levels after statin treatment is unclear. METHODS: Subjects included 985 patients at high risk of cardiovascular disease who had taken statins for more than 6 months. FLDL-C data were compared to DLDL-C data. RESULTS: A strong correlation was observed between DLDL-C and FLDL-C data (R2=0.879). However, the absolute values for FLDL-C and DLDL-C differed significantly according to a paired t-test, and 42.3% of patients showed a difference of greater than 10% between these two values. Among patients with diabetes, the percentage of patients deemed to have achieved target LDL-C levels differed significantly according to the method of LDL-C determination (p=0.007). CONCLUSIONS: FLDL-C and DLDL-C data remained well correlated after statin treatment, although the absolute values differed significantly according to the LDL-C determination method. Furthermore, the percentage of subjects deemed to achieve target LDL-C levels differed significantly according to the method of determination among patients with diabetes.
Cardiovascular Diseases ; Cholesterol ; Cholesterol, LDL ; Diabetes Mellitus ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoproteins ; Triglycerides