Biomarkers ; metabolism ; Cholesterol ; metabolism ; Coronary Disease ; Humans

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

The nature of the resistance in the rat to the development of experimental atherosclerosis is unknown, and its elucidation on mechanisms is vital to further knowledge of the pathogenesis of the disease. The liver is the main organ where cholesterol synthesis predominantly occurs and is also the main source for the plasma cholesterol. One of the factors which regulates the cholesterol metabolism is the thyroid hormone, that is a well known fact. Therefore, with combination of partial hepatectomy and administration of thiouracil, alteration of tissue lipid distribution was studied. 1. Exogenous high cholesterol feeding did not elevate the total serum cholesterol and partial hepatectomized rats, but did cause significant alterations in the tissue lipid distribution. particularly in the adrenal gland, small intestine, liver and kidney. The thyroid gland became hyperplastic. 2. The combined administration of Tapazole and cholesterol caused only a slight elevation of the serum cholesterol level as compared with that of controls, but very significant alterations in the tissue lipid distribution in the adrenal gland and liver. 3. The combined administration of Thyroxine and cholesterol caused only a tendency to minimal decrement of serum cholesterol level as compard with that of controls, but produced a significant inhibition of tissue lipid accumulation in the liver and kidney. 4. Partial hepatectomy caused neither the changes in serum cholesterol level, nor effect of the tissue lipid distribution. 5. Lipid accumulation in the coronary artery and aorta could not be demonstrated, although there was some alteration in the serum cholesterol level and in the tissue lipid distributon. It appears that, in the rats, there was no particular alteration of the intestinal absorption of cholesterol regardless of the thyroid status, and in the pathways of cholesterol metabolism after absorption, partial hepatectomy did not induce particular effect, but changes in the thyroid function did show measurable effects. However, the fact that there were no significant elevations in the serum cholesterol and tissue lipid in the liver suggests that homeostatic mechanisms may have a greater role in the high resistance to the development of atherosclerosis than does an actively functioning thyroid gland.
Animals ; Cholesterol/*metabolism ; *Hepatectomy ; Hypothyroidism/*metabolism ; Lipids/*metabolism ; Male ; Rats

BACKGROUND: Several biologically plausible mechanisms have been proposed for estrogen-associated changes in lipid and bone metabolism. These effects are thought to be mediated via estrogen receptor (ER). Several polymorphisms in the gene encoding estrogen receptor alpha may modify the effects of hormone replacement therapy on lipid and bone density in postmenopausal women. METHODS: We examined 284 postmenopausal women for thymine-adenine (TA) repeat polymorphism at the ER gene locus and its relationship to lipid and bone density. Their mean age was 52.2+/-5.0 years. We also investigated the association between ER TA repeat polymorphism and changes in lipid and bone density after 3 months and 1 year of hormone replacement therapy. RESULTS: According to the mean number of TA repeats, the women were divided into two groups: group H, with higher number of repeats (TA>16)(n=110); group L, with lower number of repeats (TAcholesterol levels after 3 month hormone replacement therapy than in group H (changes in total cholesterol: -8.4+/-11.3% vs. -4.2+/-12.5%, p=0.019), (changes in LDL cholesterol: -18.7+/-18.4% vs -8.8+/-30.1%, p=0.006). There was no significant relationship between TA repeat polymorphism and changes in HDL cholesterol, triglyceride levels and bone density after 1 year hormone replacement therapy. CONCLUSION: These data suggest that ER TA repeat polymorphism may be one of the predictors of lipid response to hormone replacement therapy.
Bone Density* ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Estrogen Receptor alpha ; Estrogens* ; Female ; Hormone Replacement Therapy* ; Humans ; Metabolism ; Receptors, Estrogen ; Triglycerides

BACKGROUND AND OBJECTIVES: In this study we investigated the association between the polymorphism of apolipoprotein E and the development of myocardial infarction, and assessed whether this polymorphism produces any changes of plasma lipid level. SUBJECTS AND METHODS: A total of 182 patients participated in this study and were divided into two groups; 91 patients with myocardial infarction (MI group) and 91 patients with no known heart disease (control group). For both groups we analyzed the clinical parameters, the changes of plasma lipid level and the degree of polymorphism of apolipoprotein E. RESULTS: Total cholesterol, triglyceride and LDL cholesterol levels were significantly higher in the MI group, while the HDL cholesterol level was significantly lower. Compared with the control group, the frequency of epsilon2 allele was significantly lower while that of epsilon3 allele was significantly higher in the MI group. As for the control group, the triglyceride level was significantly higher in the patients with epsilon 2 allele than in those without epsilon 2 allele, and the total cholesterol level was significantly higher in the patients with epsilon 4 allele than in those without epsilon 4 allele. In the MI group, the plasma lipid levels were not significantly different from those in the control group. CONCLUSION: We suggested that apolipoprotein E polymorphism could affect the lipid metabolism as well as the development of myocardial infarction. However further study is needed in patients with myocardial infarction.
Alleles ; Apolipoproteins E ; Apolipoproteins* ; Cholesterol ; Cholesterol, HDL ; Cholesterol, LDL ; Heart Diseases ; Humans ; Lipid Metabolism ; Lipoproteins ; Myocardial Infarction* ; Plasma ; Triglycerides

The lipids present in hepatic stellate cells (HSCs) lipid droplets include retinyl ester, triglyceride, cholesteryl ester, cholesterol, phospholipids and free fatty acids. Activation of HSCs is crucial to the development of fibrosis in liver disease. During activation, HSCs transform into myofibroblasts with concomitant loss of their lipid droplets and production of excessive extracellular matrix. Release of lipid droplets containing retinyl esters and triglyceride is a defining feature of activated HSCs. Accumulating evidence supports the proposal that recovering the accumulation of lipids would inhibit the activation of HSCs. In healthy liver, quiescent HSCs store 80% of total liver retinols and release them depending on the extracellular retinol status. However, in injured liver activated HSCs lose their retinols and produce a considerable amount of extracellular matrix, subsequently leading to liver fibrosis. Further findings prove that lipid metabolism of HSCs is closely associated with its activation, yet relationship between activated HSCs and the lipid metabolism has remained mysterious.
Animals ; Cholesterol ; metabolism ; Hepatic Stellate Cells ; physiology ; Humans ; Lipid Metabolism ; Triglycerides ; metabolism ; Vitamin A ; metabolism

To explore the anti-atherosclerotic mechanism of estrogen and especially observe the effect of estradiol on the content of cholesterol in J774a.1 mouse mononuclear/macrophage-derived foam cells which were incubated with oxidized low-density lipoproteins (ox-LDL). J774a.1 mouse mononuclear/macrophages were incubated with ox-LDL or with both ox-LDL and estradiol (1, 0.1 or 0.01 micromol x L(-1)). Oil red O staining was used to observe the formation of foam cells, and cholesterol oxidase fluorometric was used to determine the content of cellular cholesterol content. Western blotting and RTFQ-PCR were used to observe the expressions of scavenger receptor class B type I (SR-B I ) in J774a.1 foam cells. Compared with the control cells, J774a.1 mouse mononuclear/macrophage-derived foam cells showed significantly increased contents of total cholesterol and cholesterol ester (P < 0.001) and decreased SR-B I mRNA expression (P < 0.01). Estradiol treatment significantly lowered the contents of total cholesterol and cholesterol ester (P < 0.05), and increased SR-B I protein and mRNA expression (P < 0.01) in the foam cells in a dose-dependent manner. Estradiol can inhibit the formation of mononuclear/macrophage-derived foam cells by decreasing the contents of total cholesterol and cholesterol ester and up-regulating the expression of SR-B I in the foam cells.
Animals ; Cell Line ; Cholesterol ; metabolism ; Cholesterol Esters ; metabolism ; Estradiol ; pharmacology ; Foam Cells ; cytology ; metabolism ; Lipoproteins, LDL ; metabolism ; Macrophages ; drug effects ; metabolism ; Mice ; Scavenger Receptors, Class B ; metabolism

No abstract available.
Cholesterol* ; Female ; Hypertension, Pregnancy-Induced* ; Lipoproteins* ; Metabolism* ; Pregnancy ; Pregnancy*

Pancreatic cancer has an insidious onset and lacks effective treatment methods, which is one of the tumors with the worst prognosis, so it is urgent to explore new treatment directions. Metabolic reprogramming is one of the important hallmarks of tumors. Pancreatic cancer cells in the harsh tumor microenvironment have comprehensively increased cholesterol metabolism in order to maintain strong metabolic needs, and cancer associated fibroblasts also provide cancer cells with a large amount of lipids. Cholesterol metabolism reprogramming involves the changes in the synthesis, uptake, esterification and metabolites of cholesterol, which are closely related to the proliferation, invasion, metastasis, drug resistance, and immunosuppression of pancreatic cancer. Inhibition of cholesterol metabolism has obvious anti-tumor effect. In this paper, the important effects and complexity of cholesterol metabolism in pancreatic cancer were comprehensively reviewed from perspectives of risk factors for pancreatic cancer, energy interaction between tumor-related cells, key targets of cholesterol metabolism and its targeted drugs. Cholesterol metabolism has a strict regulation and feedback mechanism, and the effect of single-target drugs in clinical application is not clear. Therefore, multi-target therapy of cholesterol metabolism is a new direction for pancreatic cancer treatment.
Humans ; Pancreatic Neoplasms/pathology* ; Cholesterol/metabolism* ; Tumor Microenvironment

Cholesterol is an important lipid in the body of mammals and an essential component of membrane structures. Cholesterol homeostasis is critical for the maintenance of cellular and body activities, and is mainly regulated by the balance of cholesterol biosynthesis and the exogenous cholesterol uptake. Aberrantly regulated cholesterol metabolism promotes tumor cell proliferation，survival，invasion and metastasis，and their adaptability into the tumor microenvironment. Therefore，targeting cholesterol biosynthesis and reduction of plasma cholesterol levels and cholesterol esterification will provide new strategies for cancer treatment. This review summarizes the current understanding in cholesterol homeostasis regulation and its function in the occurence and development of cancer，as well as current metabolism-targeted cancer treatments.
Animals ; Cell Proliferation ; Cholesterol ; Homeostasis ; Lipid Metabolism ; Neoplasms ; Tumor Microenvironment