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

OBJECTIVETo investigate effects of serum HDL(1) on the formation of foam cells from human peripheral blood monocyte-derived macrophages.

METHODSSectie density polyacrylamide gel electrophoresis (sd-PAGE) was applied for isolation and preparation of HDL(1) simultaneously. Monocytes were isolated from human peripheral blood by Ficoll-Hypaque density gradient centrifugation and plastic adsorptive process. The isolated monocytes were stimulated by phorbol 12-myristate 13-acetate (PMA) at a concentration of 50 nmol/L for 48 h and transferred to macrophages. The monocyte-derived macrophages were then coincubated with 80 mg/L ox-LDL and HDL(1) (0, 0.1, 1.0 and 10.0 mg/L) for 6, 12 and 24 h, respectively. The formation of foam cells was identified by transmission electron microscope (TEM), total cholesterol (TC), free cholesterol (FC) and protein (Pro) in cultured cells were quantitatively analyzed by high performance chromatography (HPLC) and modified lowry protein assay, respectively.

RESULTSHDL(1) isolated from human serum by sd-PAGE could significantly decrease TC/Pro ratio in foam cells in a concentration-dependent (0 mg/L: 36.9 +/- 1.1, 10.0 mg/L: 6.2 +/- 0.4, P < 0.01) and time-dependent (10.0 mg/L HDL(1) 6 h: 16.9 +/- 0.9, 24 h: 6.4 +/- 0.6, P < 0.01) manner.

CONCLUSIONHDL(1) is capable of inhibiting and attenuating the formation of foam cells by decreasing cellular TC, therefore, might play an important role in attenuating atherosclerosis.

Atherosclerosis ; Cells, Cultured ; Cholesterol, LDL ; metabolism ; Foam Cells ; cytology ; metabolism ; Humans ; Lipoproteins, HDL ; blood ; Lipoproteins, LDL ; Monocytes ; cytology ; metabolism

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

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 (TALDL cholesterol 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

PURPOSE: Proprotein convertase subtilisin/kexin type 9 (PCSK9) binds to the low density lipoprotein receptor (LDLR) and promotes degradation of the LDLR. Inhibition of PCSK9 either by reducing its expression or by blocking its activity results in the upregulation of the LDLR and subsequently lowers the plasma concentration of LDL-cholesterol. As a modality to inhibit PCSK9 action, we searched the chemical library for small molecules that block the binding of PCSK9 to the LDLR. MATERIALS AND METHODS: We selected 100 chemicals that bind to PCSK9 where the EGF-AB fragment of the LDLR binds via in silico screening of the ChemBridge chemical library, using the computational GOLD algorithm analysis. Effects of chemicals were evaluated using the PCSK9-LDLR binding assay, immunoblot analysis, and the LDL-cholesterol uptake assay in vitro, as well as the fast performance liquid chromatography assay for plasma lipoproteins in vivo. RESULTS: A set of chemicals were found that decreased the binding of PCSK9 to the EGF-AB fragment of the LDLR in a dose-dependent manner. They also increased the amount of the LDLR significantly and subsequently increased the uptake of fluorescence-labeled LDL in HepG2 cells. Additionally, one particular molecule lowered the plasma concentration of total cholesterol and LDL-cholesterol significantly in wild-type mice, while such an effect was not observed in Pcsk9 knockout mice. CONCLUSION: Our findings strongly suggest that in silico screening of small molecules that inhibit the protein-protein interaction between PCSK9 and the LDLR is a potential modality for developing hypercholesterolemia therapeutics.
Animals ; Cholesterol/*blood ; Cholesterol, LDL/blood ; Hep G2 Cells ; Humans ; Mice ; Mice, Knockout ; Proprotein Convertases/*metabolism ; Receptors, LDL/*metabolism ; Serine Endopeptidases/*metabolism ; *Small Molecule Libraries

OBJECTIVETo investigate if inflammatory stress enhances liver lipid accumulation via SREBPs mediated dysregulation of low density protein receptor (LDLr) expression in apolipoprotein E, scavenger receptors class A and CD36 triple knockout (ApoE/SRA/CD36 KO) mice.

METHODS16 Male ApoE/SRA/CD36 KO mice were subcutaneously injected with 0.5 ml 10% casein or PBS. The mice were fed a Western diet (Harlan, TD88137) containing 21% fat and 0.15% of cholesterol for 14 weeks. Animals were sacrificed and blood samples were collected. The serum amyloid A (SAA), IL-6, total cholesterol (TC), LDL and high density protein (HDL) were assayed. The lipid accumulation in liver was evaluated by Oil Red O staining. The mRNA and protein expression of SREBP-2, SREBPs cleavage activating protein (SCAP) and LDLr were analyzed by Real-Time Polymerase Chain Reaction (RT-PCR) and immunohistochemistry staining.

RESULTSBlood levels of SAA [(26.60+/-3.24) ng/ml vs (14.35+/-1.73) ng/ml, P < 0.01] and IL-6 [(36.37+/-2.20) pg/ml vs (18.02+/-4.87) pg/ml, P < 0.01] were higher, while TC [(7.72+/-1.70) mmol/L vs (13.23+/-3.61)mmol/L, P less than 0.01], LDL-cholesterol [(2.94+/-0.44) mmol/L vs (9.28+/-3.66) mmol/L, P less than 0.01] and HDL cholesterol [(2.24+/-0.63) mmol/L vs (4.13+/-0.42) mmol/L, P less than 0.01] were lower in inflamed mice compared to controls. ORO staining showed that lipid accumulation in the liver was more extensive in inflamed group despite lower blood lipid levels. Meanwhile, Real Time PCR data showed inflammation induced the expression of LDLr (4.56 fold), SCAP (3.14 fold) and SREBP-2 (14.72 fold) in liver. Immunohistochemical staining also indicated increased proteins expression in the liver, which was consistent with mRNA data.

CONCLUSIONSInflammation causes lipid accumulation in liver via disrupting SREBP-2 and LDLr expression.

Animals ; Apolipoproteins E ; genetics ; Cholesterol, LDL ; metabolism ; Fatty Liver ; metabolism ; Inflammation ; metabolism ; Liver ; metabolism ; Male ; Mice ; Mice, Knockout ; Receptors, LDL ; metabolism ; Sterol Regulatory Element Binding Protein 2 ; metabolism

The role of very low density lipoprotein receptor (LVLDR) in the process of foam cell formation was investigated. After the primary cultured mouse peritoneal macrophages were incubated with VLDL, beta-VLDL or low density lipoprotein (LDL), respectively for 24 h and 48 h, foam cells formation was identified by oil red O staining and cellular contents of triglyceride (TG) and total cholesterol (TC) were determined. The mRNA levels of LDLR, LDLR related protein (ILRP) and VLDLR were detected by semi-quantitative RT-PCR. The results demonstrated that VLDL, beta-VLDL and LDL could increase the contents of TG and TC in macrophages. Cells treated with VLDL or beta-VLDL showed markedly increased expression of VLDLR and decreased expression of LDLR, whereas LRP was up-regulated slightly. For identifying the effect of VLDL receptor on cellular lipid accumulation, ldl-A7-VR cells, which expresses VLDLR and trace amount of LRP without functional LDLR, was used to incubate with lipoproteins for further examination. The results elucidated that the uptake of triglyceride-rich lipoprotein mediated by VLDLR plays an important role in accumulation of lipid and the formation of foam cells.
Animals ; Arteriosclerosis ; metabolism ; pathology ; Cells, Cultured ; Cholesterol, LDL ; metabolism ; pharmacology ; Female ; Foam Cells ; cytology ; metabolism ; Lipoproteins, VLDL ; pharmacology ; Macrophages, Peritoneal ; cytology ; metabolism ; Mice ; Receptors, LDL ; metabolism ; Triglycerides ; 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

BACKGROUND: In postmenopausal women, progestogen should be added to protect the endometrium from hyperplasia or carcinoma induced by the unopposed estrogen. However, the effects of progestogen on bone mineral densities and serum lipodproteins have not been precisely evaluated in Korean postmenopausal women. METHODS: To evaluate the effects of progestogen on bane mineral densities and serum lipoprotein in estrogen rephcement therapy, we canducted a 2-year trial of long conjugated equine estrogen(conjugated estrogen 0.625mg/day) with or without cyclic progestogen(MPA 5mg/day for 12 days) in 120 postmenopausal women. In all subjects, bone mineral density was measured in lumbar vertebra(L2-L4) and femur neck using dual energy X-ray absorptiometry(DEXA) and serum lipoprotein was measured from the beginning of the treatment, 12 manths, and 24 manths later, respectively. RESULTS: BMD of femur neck in both groups increased but not significantly compared to basal level at 12 months and/or 24 months of treatment. As for BMD of lumbar spine, it increased significantly in both groups. Both groups showed a significant decrease in the levels LDL cholesterol, but there was no statistical significance in serum triglycerids. Conjugated estrogen plus MPA group in constrast to conjugated estrogen only group showed a significant decrease in total cholesterol levels. CONCLUSIONS: These results suggest that the addition of MPA of the daily of 5mg for 12 days cyclically in estrogen replacement treatment appear to be effective in postmenopausal women with protection on bone mineral density and maintenance of long-term favorable effects on serum lipoprotein.
Bone Density* ; Cholesterol ; Cholesterol, LDL ; Endometrium ; Estrogen Replacement Therapy* ; Estrogens* ; Female ; Femur Neck ; Humans ; Hyperplasia ; Lipid Metabolism* ; Lipoproteins ; Postmenopause ; Spine

Objective: To investigate the effect of pesticides and herbicides on lipid metabolism. Methods: In November 2020, Based on the data of the national health and Nutrition Survey (NHANES) (2011-2014) , select the population aged 20~65 who have demographic information, pesticide use and data of four lipid metabolism indicators [total cholesterol (TC) , triglyceride (TG) , high density lipoprotein cholesterol (HDLC) and low density lipoprotein cholesterol (LDLC) ] (n=3039) . The subjects were divided into insecticide group (320 people) and non insecticide group (2719) according to the use of insecticides, and herbicide group (156 people) and non herbicide group according to the use of herbicides. Results: Among the 3039 subjects, the males and female were 1509 (49.7%) and 1530 (50.3%) respectively. The males age was (39.7±12.0) years and the females age was (40.2±12.0) years The concentration of HDLC in the NHANES (55.4±15.0) mg/dl was lower than that of (58.2±14.2) mg/dL in the non herbicide group (P<0.05) (b=-0.044, P<0.05) . The results showed that the use of herbicides was related to the decrease of HDLC and the increase of LDLC and LDLC/HDLC in female population (b=-0.050, 0.062, 0.067, all P<0.05) . Conclusion: Herbicide exposure can cause the change of lipid metabolism, and the effect on female population is more obvious.
Adult ; Cholesterol, HDL ; Cholesterol, LDL ; Female ; Humans ; Lipid Metabolism ; Male ; Middle Aged ; Nutrition Surveys ; Pesticides ; Young Adult