Calcium/vitamin D supplementation, serum 25-hydroxyvitamin D concentrations, and cholesterol profiles in the Women’s Health Initiative calcium/vitamin D randomized trial
Peter F. SchnatzXuezhi JiangSharon Vila-WrightAaron K. AragakiMatthew NudyDavid M. O’SullivanRebecca D. JacksonErin S. LeBlancJennifer G. RobinsonJames M. ShikanyCatherine WomackLisa W. MartinMarian L. NeuhouserMara Z. VitolinsYiqing SongStephen B. KritchevskyJoAnn E. Manson
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The objective of this study was to evaluate whether increased serum 25-hydroxyvitamin D3 (25OHD3) concentrations, in response to calcium/vitamin D (CaD) supplementation, are associated with improved lipids in postmenopausal women.Keywords:
Lipid Profile
High-density lipoprotein
Lipoprotein (a) (Lp(a)) and other lipid values have been correlated with angiographically defined [table: see text] coronary artery disease. To study this relationship in Indian patients, plasma levels of Lipoprotein (a) and other lipids were assessed in 74 patients undergoing Coronary arteriography and also in 53 age and sex matched healthy male blood bank donors who served as controls. Total cholesterol (mg/dl) (211 +/- 56 vs 186 +/- 43; p < 0.001), low density lipoprotein Cholesterol (mg/dl) (117 +/- 40 vs 88 +/- 29; p > 0.001) and low density lipoprotein/high density lipoprotein cholesterol ratio (2.6 +/- 0.8 vs 2.2 +/- 0.9; p < .001) were significantly higher in patients than controls. High density lipoprotein-cholesterol (mg/dl) (43.5 +/- 6 vs 42.1 +/- 7; p-ns) very low density lipoprotein-cholesterol (mg/dl) (49.7 +/- 17 vs 56.1 +/- 25; p-ns) and triglycerides (mg/dl) (155 +/- 101 vs 167 +/- 88; p-ns) were not statistically different in two groups. Lipoprotein (a) levels showed highly skewed distribution. Patients (n = 74) showed almost five fold higher lipoprotein (a) levels (mg/dl) as compared to controls (n = 53) [105 +/- 565 vs 23 +/- 76]. Patients with very high lipoprotein (a) levels [values of more than 40 mg/dl] (n = 18) had high density lipoprotein cholesterol and total cholesterol significantly lower than rest of the patient group. [high density lipoprotein cholesterol (mg/dl) 41.00 +/- 3.7 vs 44 +/- 6.4; p < 0.01 and total cholesterol (mg/dl) 192 +/- 34 vs 217 +/- 53; p < 0.05].
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Background Recently, several studies have shown that microRNAs are present in high-density lipoprotein, and high-density lipoprotein-microRNA may be a promising disease biomarker. We investigated the stability of high-density lipoprotein-microRNAs in different storage conditions as this is an important issue for its application to the field of clinical research. Methods microRNAs were extracted from the high-density lipoprotein fraction that was purified from the serum. miR-135 a and miR-223, which are known to be present in high-density lipoprotein, were quantified by quantitative real-time PCR. The influence of preanalytical parameters on the analysis of high-density lipoprotein-miRNAs was examined by the effect of RNase, storage conditions, and freezing and thawing. Results The concentrations of microRNA in high-density lipoprotein were not altered by RNase A treatment (0–100 U/mL). No significant change in these microRNAs was observed after storing serum at room temperature or 4℃ for 0–24 h, and there was a similar result in the cryopreservation for up to two weeks. Also, high-density lipoprotein-microRNAs were stable for, at least, up to five freeze–thaw cycles. Conclusions These results demonstrated that high-density lipoprotein-microRNAs are relatively resistant to various storage conditions. This study provides new and important information on the stability of high-density lipoprotein-microRNAs.
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The substrate specificity of lipid transfer protein has been examined in whole plasma in vitro by following the redistribution of high density lipoprotein (HDL)-derived [3H]cholesteryl ester (CE) into apolipoprotein (apo) B-containing lipoproteins using density gradient ultracentrifugation. HDL-derived [3H]CEs were incubated with plasma or isolated lipoprotein classes (very low density lipoprotein, intermediate density lipoprotein, and low density lipoprotein [LDL] subpopulations from the HDL donor) with and without lipoprotein lipase for 0.5-6 hours at 37 degrees C. After incubation, lipoproteins were separated into 38 fractions after density gradient ultracentrifugation, and radioactivity, protein, and cholesterol were monitored across the profiles. These studies indicate that 1) lipid transfer protein activity varied among the individuals as well as within an individual; 2) the majority of the [3H]CE was associated with LDL; 3) in most individuals (71%), more HDL-derived [3H]CE distributed within the buoyant LDL density region; and 4) the distribution of HDL-derived [3H]CE was similar to the distribution of lipoprotein lipase-derived "remnant" particles within buoyant LDL. These in vitro studies support the hypothesis that HDL-derived [3H]CEs vary in their distribution among apo B-containing particles and that more HDL-derived [3H]CEs are transferred to lipoproteins within the buoyant LDL density range. Additional studies suggest that lipoprotein heterogeneity within this density range, such as the presence of remnant-like lipoproteins, may contribute to the selective distribution of HDL-derived [3H]CE into buoyant LDL.
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Effects of chronic ethanol consumption on serum lip-oproteins have been studied in the rat. The serum levels of triglycerides, cholesterol, phospholipids and apolipo-proteins AI and AIV increased significantly after 1 week of ethanol feeding, and they remained elevated up to 7 weeks of alcohol drinking. By contrast, serum total apolipoprotein E decreased or, sometimes, did not change. Very-low-density lipoprotein cholesterol, triglycerides and very-low-density lipoprotein apolipoprotein E of the alcohol-fed rats increased in parallel and were about 2-to 2.5-fold over the controls. Whereas high-density lipoprotein cholesterol, phospholipids, apolipoprotein AI and AIV increased 1.2-fold by chronic alcohol feeding, the level of high-density lipoprotein apolipoprotein E decreased to 70% of that of the control rats. The rates of secretion of apolipoprotein AI, E and AIV into the culture medium by hepatocytes isolated from ethanol-fed rats were 1.8-, 1.3-and 1.1-fold higher than those from control rats. These data indicate that (i) chronic ethanol feeding increases very-low-density lipoprotein and high-density lipoprotein in the rat; (ii) serum high-density lipoprotein particles of the ethanol-fed rats are deficient in apolipoprotein E, and (iii) chronic ethanol feeding increases hepatic secretion of apolipoprotein AI, E and AIV. Since the steady-state serum level of apolipoprotein E decreases or remains unchanged in the presence of increased hepatic apolipoprotein E secretion, this imbalance suggests that alcohol feeding either accelerates the rate of degradation of serum apolipoprotein E or suppresses apolipoprotein E synthesis by nonhepatic tissues.
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We determined serum high-density lipoprotein cholesterol content and analyzed the apoprotein structure of the various lipoprotein fractions in 21 patients on chronic hemodialysis. High-density lipoprotein cholesterol was significantly reduced in all patients as compared with 11 normal persons (mean ±1 standard deviation: 26±13 vs. 52±9 mg per 100 ml; P<0.001) whether or not triglyceride levels were raised. In seven of those with Type IV hyperlipoproteinemia, protein content of high-density lipoprotein and its subfractions 1, 2 and 3 were also reduced (P<0.001) in parallel with reductions in cholesterol in these fractions. Apoprotein electrophoresis showed an increase in "arginine-rich" peptide in very-low-density lipoprotein and high-density lipoprotein fraction 1, and a reduction in apoprotein CII in very-low-density and high-density lipoprotein. In addition to their reduced high-density lipoprotein cholesterol levels, a major factor in the atherosclerosis of these patients may be their abnormal high-density lipoprotein composition. Their raised triglyceride levels could be due to defective lipoprotein lipase activation by the reduced very-low-density lipoprotein apoprotein CII. (N Engl J Med 299:1326–1329, 1978)
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The most accepted property of high-density lipoprotein is reverse cholesterol transport. However, other beneficial actions may contribute to the antiatherogenic role of high-density lipoprotein. This review addresses the action of high-density lipoprotein beyond reverse cholesterol transport.High-density lipoprotein cholesterol levels are inversely associated with coronary heart disease and other forms of vascular disease. Apart from transferring excess cholesterol to the liver, high-density lipoprotein exhibits favorable effects on oxidation, inflammation, thrombosis and endothelial function. Some of these actions are at least in part attributed to high-density lipoprotein-associated enzymes, such as paraoxonase and platelet-activating factor acetylhydrolase. However, high-density lipoprotein can become dysfunctional and proatherogenic under certain circumstances.Current data suggest that high-density lipoprotein possesses various properties beyond reverse cholesterol transport. However, many issues on the exact role of high-density lipoprotein remain unknown. Future research is needed.
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