1.Higher High Density Lipoprotein 2 (HDL2) to Total HDL Cholesterol Ratio Is Associated with a Lower Risk for Incident Hypertension
You Cheol HWANG ; Wilfred Y FUJIMOTO ; Steven E KAHN ; Donna L LEONETTI ; Edward J BOYKO
Diabetes & Metabolism Journal 2019;43(1):114-122
BACKGROUND: Recent studies have suggested that high density lipoprotein (HDL) cholesterol is inversely associated with the development of hypertension. We aimed to determine the association between different HDL cholesterol subclasses and risk of future hypertension. METHODS: A total of 270 Japanese Americans (130 men, 140 women) without hypertension between the ages of 34 to 75 years were enrolled. Blood pressure was measured with a mercury sphygmomanometer, and average blood pressure was calculated. Incident hypertension was determined 5 to 6 and 10 to 11 years after enrollment. HDL2, HDL3, and total HDL cholesterol were measured at baseline. RESULTS: During 10 years of follow-up, the cumulative incidence of hypertension was 28.1% (76/270). In univariate analysis, age, diabetes, waist circumference, systolic and diastolic blood pressure, fasting glucose, insulin resistance index, total and low density lipoprotein cholesterol, and visceral adipose tissue were significant predictors for incident hypertension. Among the HDL cholesterol subclass, HDL2 cholesterol was inversely associated with hypertension incidence, but both total and HDL3 cholesterol were not. In addition, HDL2/HDL cholesterol was inversely associated with future hypertension risk. In multivariate analysis, age (odds ratio [OR], 1.71; 95% confidence interval [CI], 1.26 to 2.31; P=0.001), systolic blood pressure (OR, 1.83; 95% CI, 1.31 to 2.56; P < 0.001), and HDL2/HDL cholesterol (OR, 0.71; 95% CI, 0.52 to 0.98; P=0.035), were associated with future development of hypertension. CONCLUSION: A higher proportion of HDL2 cholesterol among total HDL cholesterol predicted a lower risk for incident hypertension. However, concentrations of total HDL, HDL2, and HDL3 cholesterol were not independent predictors of incident hypertension.
Asian Americans
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Blood Pressure
;
Cholesterol
;
Cholesterol, HDL
;
Cholesterol, LDL
;
Fasting
;
Follow-Up Studies
;
Glucose
;
Humans
;
Hypertension
;
Incidence
;
Insulin Resistance
;
Intra-Abdominal Fat
;
Lipoproteins
;
Lipoproteins, HDL2
;
Lipoproteins, HDL3
;
Male
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Multivariate Analysis
;
Sphygmomanometers
;
Waist Circumference
3.Antioxidative Activity after Rosuvastatin Treatment in Patients with Stable Ischemic Heart Disease and Decreased High Density Lipoprotein Cholesterol.
Do Sim PARK ; Kyeong Ho YUN ; Hyun Young PARK ; Sang Jae RHEE ; Nam Ho KIM ; Seok Kyu OH ; Jin Won JEONG
Korean Circulation Journal 2016;46(3):309-314
BACKGROUND AND OBJECTIVES: The clinical significance of statin-induced high-density lipoprotein cholesterol (HDL-C) changes is not well known. We investigated whether rosuvastatin-induced HDL-C changes can influence the anti-oxidative action of high-density lipoprotein particle. SUBJECTS AND METHODS: A total of 240 patients with stable ischemic heart disease were studied. Anti-oxidative property was assessed by paraoxonase 1 (PON1) activity. We compared the lipid profile and PON1 activity at baseline and at 8 weeks after rosuvastatin 10 mg treatment. RESULTS: Rosuvastatin treatment increased the mean HDL-C concentration by 1.9±9.2 mg/dL (6.4±21.4%). HDL-C increased in 138 patients (57.5%), but decreased in 102 patients (42.5%) after statin treatment. PON1 activity increased to 19.1% in all patients. In both, the patients with increased HDL-C and with decreased HDL-C, PON1 activity significantly increased after rosuvastatin treatment (+19.3% in increased HDL-C responder; p=0.018, +18.8% in decreased HDL-C responder; p=0.045 by paired t-test). Baseline PON1 activity modestly correlated with HDL-C levels (r=0.248, p=0.009); however, the PON1 activity evaluated during the course of the treatment did not correlate with HDL-C levels (r=0.153, p=0.075). CONCLUSION: Rosuvastatin treatment improved the anti-oxidative properties as assessed by PON1 activity, regardless of on-treatment HDL-C levels, in patients with stable ischemic heart disease.
Aryldialkylphosphatase
;
Cholesterol
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Cholesterol, HDL*
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Humans
;
Hydroxymethylglutaryl-CoA Reductase Inhibitors
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Lipoproteins
;
Lipoproteins, HDL
;
Myocardial Ischemia*
;
Rosuvastatin Calcium*
5.Correlation between GPR, MHR and elderly essential hypertension with unstable angina pectoris.
Xiaoteng LIU ; Ying ZHANG ; Fengbiao JIN ; Huiqing LIU ; Qinglian LI ; Yu GAO ; Ruitian HOU ; Zhimin ZHANG
Journal of Central South University(Medical Sciences) 2021;46(4):373-378
OBJECTIVES:
To investigate the level and significance of serum γ-glutamyl transferase-to-platelet ratio (GPR) and monocyte count to high-density lipoprotein ratio (MHR) in patients with essential hypertension (EH) and unstable angina (UA).
METHODS:
A total of 218 patients with coronary angiography aged ≥60 years, who were admitted to the EH hospital of the Department of Cardiac Medicine, Affiliated Hospital of Chengde Medical College, were selected from September 2018 to September 2019. They were divided into an EH+UA group (
RESULTS:
Compared with the control group, patients in the EH+UA group and the EH group had higher body mass index (BMI), tyiglyceride (TG), GPR, and MHR, and lower high-density lipoprotein-cholesterol (HDL-C) (all
CONCLUSIONS
There is a correlation between GPR, MHR and EH combined with UA pectoris, and the combined detection of the two indicators has adjuvant diagnostic value for elderly EH combined with UA.
Aged
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Angina, Unstable
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Cholesterol, HDL
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Coronary Angiography
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Essential Hypertension
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Humans
;
Lipoproteins, HDL
;
Monocytes
6.Advances in clinical significance and detection methods research of high density lipoprotein subfractions.
Chao Juan WEN ; Min Hong WANG ; Pei YU ; Qiang ZHOU
Chinese Journal of Preventive Medicine 2023;57(11):1901-1907
High density lipoprotein (HDL) is an important biochemical index of clinical cardiovascular disease. Many new studies have demonstrated abnormalities of plasma HDL subfractions in patients with this disease,and their clinical significance is greater than the overall abnormalities of HDL. Therefore,the HDL subfraction as an important factor in cardiovascular disease has attracted extensive research and attention. This article summarizes current research on HDL subfractions,their measurements and their relationships with atherosclerosis and coronary artery disease.
Humans
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Cardiovascular Diseases
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Clinical Relevance
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Cholesterol, HDL
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Lipoproteins, HDL
;
Coronary Artery Disease
7.Advances in clinical significance and detection methods research of high density lipoprotein subfractions.
Chao Juan WEN ; Min Hong WANG ; Pei YU ; Qiang ZHOU
Chinese Journal of Preventive Medicine 2023;57(11):1901-1907
High density lipoprotein (HDL) is an important biochemical index of clinical cardiovascular disease. Many new studies have demonstrated abnormalities of plasma HDL subfractions in patients with this disease,and their clinical significance is greater than the overall abnormalities of HDL. Therefore,the HDL subfraction as an important factor in cardiovascular disease has attracted extensive research and attention. This article summarizes current research on HDL subfractions,their measurements and their relationships with atherosclerosis and coronary artery disease.
Humans
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Cardiovascular Diseases
;
Clinical Relevance
;
Cholesterol, HDL
;
Lipoproteins, HDL
;
Coronary Artery Disease
8.Effect of HDL and apoAI on PGE2 production by monocyte-derived macrophages.
Xiaoqin ZHOU ; Arnold von ECKARDSTEIN
Journal of Huazhong University of Science and Technology (Medical Sciences) 2002;22(4):270-272
Effect of antiatherogenic high density lipoprotein (HDL) and apolipoprotein AI (apoAI) on production of prostaglandin E2 (PGE2) by human monocyte-derived macrophages was investigated. Macrophages were loaded with acetylated low density lipoprotein followed by incubation with HDL3 or apoAI. PGE2 produced and secreted in culture supernatant was quantified by enzyme immunoassay. HDL3 induced production of PGE2 by macrophages in a time-dependent manner. 24 h after incubation, PGE2 production by HDL3-treated macrophages increased 3.7-fold of that by control cells. ApoAI also induced PGE2 secretion to 2.1-fold, which was significantly less than HDL3. The data indicate that both HDL3 and lipid-free apoAI enhance PGE2 synthesis and secretion by human macrophages and this may further contribute to the protection from atherosclerosis.
Apolipoprotein A-I
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pharmacology
;
Arteriosclerosis
;
prevention & control
;
Culture Media, Conditioned
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Dinoprostone
;
biosynthesis
;
Humans
;
Lipoproteins, HDL
;
pharmacology
;
Lipoproteins, HDL3
;
Macrophages
;
cytology
;
metabolism
;
Monocytes
;
metabolism
9.Change of plasma lipoproteins by heparin-released lipoprotein lipase.
Jeong Yeh YANG ; Tae Keun KIM ; Bon Sun KOO ; Byung Hyun PARK ; Jin Woo PARK
Experimental & Molecular Medicine 1999;31(2):60-64
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
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Cholesterol/blood
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Heparin/pharmacology*
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Heparin/administration & dosage
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Human
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Immunoblotting
;
Lipoprotein Lipase/blood*
;
Lipoproteins/blood*
;
Lipoproteins, HDL/blood
;
Lipoproteins, LDL/blood
;
Lipoproteins, VLDL/blood
;
Triglycerides/blood
10.High-Density Lipoprotein, Lecithin: Cholesterol Acyltransferase, and Atherosclerosis.
Alice OSSOLI ; Chiara PAVANELLO ; Laura CALABRESI
Endocrinology and Metabolism 2016;31(2):223-229
Epidemiological data clearly show the existence of a strong inverse correlation between plasma high-density lipoprotein cholesterol (HDL-C) concentrations and the incidence of coronary heart disease. This relation is explained by a number of atheroprotective properties of HDL, first of all the ability to promote macrophage cholesterol transport. HDL are highly heterogeneous and are continuously remodeled in plasma thanks to the action of a number of proteins and enzymes. Among them, lecithin:cholesterol acyltransferase (LCAT) plays a crucial role, being the only enzyme able to esterify cholesterol within lipoproteins. LCAT is synthetized by the liver and it has been thought to play a major role in reverse cholesterol transport and in atheroprotection. However, data from animal studies, as well as human studies, have shown contradictory results. Increased LCAT concentrations are associated with increased HDL-C levels but not necessarily with atheroprotection. On the other side, decreased LCAT concentration and activity are associated with decreased HDL-C levels but not with increased atherosclerosis. These contradictory results confirm that HDL-C levels per se do not represent the functionality of the HDL system.
Animals
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Atherosclerosis*
;
Cholesterol*
;
Coronary Disease
;
Humans
;
Incidence
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Lecithins*
;
Lipoproteins*
;
Lipoproteins, HDL
;
Liver
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Macrophages
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Plasma
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Sterol O-Acyltransferase*