Altered high density lipoprotein metabolism in patients with myeloproliferative disorders and hypocholesterolemia
Metabolism, ISSN: 0026-0495, Vol: 35, Issue: 9, Page: 878-882
1986
- 26Citations
- 5Captures
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations26
- Citation Indexes26
- CrossRef26
- 26
- Captures5
- Readers5
Article Description
Patients with the myeloproliferative disorders (MPD), myeloid metaplasia and polycythemia vera, have significantly reduced concentrations of plasma low density (LDL) and high density (HDL) lipoprotein cholesterol (C). We have previously demonstrated that increased catabolism of LDL was associated with the low LDL-C levels. In the present study we have determined the rates of synthesis and removal of apolipoprotein A-1 (apoA-1) in five subjects with MPD who had markedly reduced HDL-C concentrations (18.2 ± 4.1 mg/dL). Their results were compared to those obtained in six subjects with hypertriglyceridemia (HTG) with similar levels of HDL-C (19.7 ± 3.9 mg/dL) and five subjects with normal (N) HDL-C concentrations (49.6 ± 7.4 mg/dL). The results demonstrated that the fractional catabolic rate (FCR) for apoA-1 was significantly increased in the MPD group v N (0.38 ± 0.15 v 0.21 ± 0.03 day −1, P < 0.05) while the synthetic rates for apoA-1 were similar in the two groups. The FCR for apoA-1 in the HTG group (0.36 ± 0.07 day −1 ) was nearly identical to that in the MPD group, in spite of the large differences in their plasma triglyceride concentrations (406.2 ± 217.9 v 117.0 ± 29.8 mg/dL, P < 0.05). Compositional studies indicated that the HTG group had very cholesterol depleted HDL while the HDL particles in the MPD group appeared to have a normal cholesterol content. These studies indicate that subjects with MPD have striking increases in HDL catabolism that can account fully for their markedly reduced levels of HDL cholesterol. The pathophysiologic mechanisms that are the basis of this alteration remain to be determined.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/0026049586902325; http://dx.doi.org/10.1016/0026-0495(86)90232-5; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0022474976&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/3747843; https://linkinghub.elsevier.com/retrieve/pii/0026049586902325; http://dx.doi.org/10.1016/0026-0495%2886%2990232-5; https://dx.doi.org/10.1016/0026-0495%2886%2990232-5
Elsevier BV
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