scholarly journals Dose-Dependent Regulation of High-Density Lipoprotein Metabolism with Rosuvastatin in the Metabolic Syndrome

2008 ◽  
Vol 93 (2) ◽  
pp. 430-437 ◽  
Author(s):  
Esther M. M. Ooi ◽  
Gerald F. Watts ◽  
Paul J. Nestel ◽  
Dmitri Sviridov ◽  
Anh Hoang ◽  
...  

Abstract Background: Low plasma concentration of high-density lipoprotein (HDL) cholesterol is a risk factor for cardiovascular disease and a feature of the metabolic syndrome. Rosuvastatin has been shown to increase HDL cholesterol concentration, but the mechanisms remain unclear. Methods and Results: Twelve men with the metabolic syndrome were studied in a randomized, double-blind, crossover trial of 5-wk therapeutic periods with placebo, 10 mg/d rosuvastatin, or 40 mg/d rosuvastatin, with 2-wk placebo washout between each period. Compared with placebo, there was a significant dose-dependent increase in HDL cholesterol, HDL particle size, and concentration of HDL particles that contain apolipoprotein A-I (LpA-I). The increase in LpA-I concentration was associated with significant dose-dependent reductions in triglyceride concentration and LpA-I fractional catabolic rate, with no changes in LpA-I production rate. There was a significant dose-dependent reduction in the fractional catabolic rate of HDL particles containing both apolipoprotein A-I and A-II (LpA-I:A-II), with concomitant reduction in LpA-I:A-II production rate, and hence no change in LpA-I:A-II concentration. Conclusions: Rosuvastatin dose-dependently increased plasma HDL cholesterol and LpA-I concentrations in the metabolic syndrome. This could relate to reduction in plasma triglycerides with remodeling of HDL particles and reduction in LpA-I fractional catabolism. The findings contribute to understanding mechanisms for the HDL-raising effect of rosuvastatin in the metabolic syndrome with implications for reduction in cardiovascular disease.


2007 ◽  
Vol 8 (1) ◽  
pp. 225
Author(s):  
E.M.M. Ooi ◽  
G.F. Watts ◽  
P.J. Nestel ◽  
D. Sviridov ◽  
A. Hoang ◽  
...  


Author(s):  
Noora Wael Rasheed ◽  
Ooroba Jameel Taresh

       Some studies indicated a relationship between increased serum levels of osteoprotegerin with arterial calcification and as a result, it leads to the risk of cardiovascular disease. In our study group we selected patients with osteoporosis, with similar age and body mass index for the assessment of the relationship between cardiovascular disease and osteoprotegerin serum level. We took into account the analysis of correlation and association between the presence of distinct patterns of atherosclerosis and associated diseases like high blood pressure,  diabetes mellitus, low HDL cholesterol, increased LDL cholesterol, increased triglycerides and was the case of presence of any type of dyslipidemia, in case of pre-existent treatment. Objective of study was the assessment of osteoprotegerin value as predictive marker for cardiovascular and metabolic risk in osteoporotic patients. Our results showed significant correlations of parathyroid hormone, osteocalcin and biochemical markers of bone with glucose metabolism and lipid were found in our research, maintaining crosstalk between calcium and biochemical markers of bone and cardiovascular risk. The serum level of Osteoprotegerin has been shown to have a large predictive value for the metabolic syndrome as a cardiovascular risk standard in patients with osteoporosis. The osteoprotegerin serum levels were increased in the patients with metabolic syndrome as a protective response facing the atherosclerotic lesions.



2009 ◽  
Vol 94 (12) ◽  
pp. 4891-4897 ◽  
Author(s):  
Laurence Duvillard ◽  
Guillaume Dautin ◽  
Emmanuel Florentin ◽  
Aline Jeannin ◽  
Jean-Paul Pais de Barros ◽  
...  

Context: The impact of estrogen plus progestin as an oral contraceptive on high density lipoprotein (HDL) apolipoprotein (apo) AI metabolism in humans is poorly understood. Objectives: This study was designed to measure the in vivo effect of Moneva (30 μg ethinylestradiol, 75 μg gestodene) on HDL apoAI production rate and fractional catabolic rate. Design: Using 13C-leucine, we performed two kinetic studies in the fed state in 10 normolipidemic young women, before and 3 months after beginning Moneva. Results: On Moneva, serum triglycerides increased by 12% (P = 0.03) in the fed state, whereas low-density lipoprotein and HDL cholesterol remained unchanged. HDL apoAI pool size and production rate were increased by 9.2% (67.3 ± 7.1 vs. 61.6 ± 6.7 mg · kg−1; P = 0.05) and 26.5% (14.3 ± 2.7 vs. 11.3 ± 2.2 mg · kg−1 · d−1; P = 0.02), respectively. HDL apoAI fractional catabolic rate was not significantly modified. Three-month treatment by Moneva induced a shift of HDL size distribution from HDL2 toward HDL3 (HDL3 = 51.5 ± 8.1 vs. 46.5 ± 9.2% of total HDL; P = 0.02) and an increase in the proportion of apoAI among HDL components (38.8 ± 4.3 vs. 34.4 ± 2.8%; P = 0.01). Conclusion: Oral contraception by estrogen plus progestin induces changes in HDL apoAI metabolism characterized by an increase in production rate and pool size, with a higher proportion of HDL3 particles. Whether or not these changes are beneficial to prevent atherosclerosis has to be explored further.



2006 ◽  
Vol 7 (3) ◽  
pp. 534
Author(s):  
J. Ji ◽  
G.F. Watts ◽  
A.G. Johnson ◽  
D.C. Chan ◽  
E.M.M. Ooi ◽  
...  


2019 ◽  
Vol 86 (2) ◽  
Author(s):  
Saúl Huerta-Ramírez ◽  
Angélica Paniagua-Pérez ◽  
David Castro-Serna ◽  
Andrés Ledesma-Velázquez ◽  
Alberto Rubio-Guerra ◽  
...  


2008 ◽  
Vol 158 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Robin P F Dullaart ◽  
Albert K Groen ◽  
Geesje M Dallinga-Thie ◽  
Rindert de Vries ◽  
Wim J Sluiter ◽  
...  

ObjectiveWe tested whether in metabolic syndrome (MetS) subjects the ability of plasma to stimulate cellular cholesterol efflux, an early step in the anti-atherogenic reverse cholesterol transport pathway, is maintained despite low high-density lipoprotein (HDL) cholesterol.DesignIn 76 subjects with and 94 subjects without MetS based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, we determined plasma (apo)lipoproteins, pre-β-HDL formation, phospholipid transfer protein (PLTP) activity, cholesterol esterification (EST), cholesteryl ester transfer (CET), adiponectin, and the ability of plasma from each subject to stimulate cholesterol efflux out of cultured fibroblasts obtained from a single donor.ResultsApo E, PLTP activity, EST, and CET were higher (P=0.04 to <0.001), whereas adiponectin was lower in MetS subjects (P<0.01). Pre-β-HDL and pre-β-HDL formation were not different between subjects with and without MetS. Cellular cholesterol efflux to plasma from MetS subjects was slightly higher versus plasma from subjects without MetS (8.8±1.0 vs 8.5±0.9%,P=0.05), but the difference was not significant after age, sex, and diabetes adjustment. Cellular cholesterol efflux was positively related to pre-β-HDL formation, EST, PLTP activity, and apo E (P<0.05 for all by multiple linear regression analysis), without an independent association with MetS and diabetes status.ConclusionsThe ability of plasma from MetS subjects to promote fibroblast cholesterol efflux is not defective, although HDL cholesterol is decreased. Higher cholesterol esterification, PLTP activity, and apo E levels may contribute to the maintenance of cholesterol efflux in MetS.



Antioxidants ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 362 ◽  
Author(s):  
Fumiaki Ito ◽  
Tomoyuki Ito

Lipid markers are well-established predictors of vascular disease. The most frequently measured lipid markers are total cholesterol, high-density lipoprotein (HDL)-cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglyceride. HDL reduces atherosclerosis by multiple mechanisms, leading to a reduced risk of cardiovascular disease, and HDL-C, as a metric of HDL quantity, is inversely associated with cardiovascular disease, independent of LDL-C. However, the quality of the HDL appears to be more important than its quantity, because HDL loses its antiatherogenic functions due to changes in its composition and becomes “dysfunctional HDL”. Although there is evidence of the existence of “dysfunctional HDL”, biomarkers for monitoring dysfunctional HDL in clinical practice have not yet been established. In this review, we propose a new lipid panel for the assessment of dysfunctional HDL and lipoprotein-related atherosclerotic cardiovascular disease. The lipid panel includes the measurement of lipid peroxide and triglyceride contents within HDL particles.



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