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Updated: Jul 13, 2026

Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Hemodialysis reduces plasma apolipoprotein C-I concentration making VLDL a better substrate for lipoprotein lipase
Insights
Hemodialysis significantly reduces apolipoprotein C-I levels, potentially improving very low-density lipoprotein (VLDL) function and triglyceride metabolism in chronic renal failure patients.
Area of Science:
- Lipid Metabolism
- Renal Disease Pathophysiology
- Biochemistry
Background:
- Apolipoprotein Cs (apoC-I, apoC-II, apoC-III) are key regulators of lipoprotein metabolism.
- Low molecular weight apoCs can be removed by dialysis membranes.
- Chronic renal failure impacts lipoprotein metabolism and enzyme activities.
Purpose of the Study:
- To investigate the effects of hemodialysis (HD) on plasma concentrations of apoCs.
- To assess the impact of HD on enzyme activities modulated by apoCs.
- To determine the clinical significance of apoC changes during HD.
Main Methods:
- Plasma samples collected from 28 chronic renal failure patients before and after HD.
- Quantification of apoC-I, apoC-II, and apoC-III levels.
- Assays for very low-density lipoprotein (VLDL) and high-density lipoprotein (HDL) associated apoCs.
- Evaluation of VLDL interaction with cholesterol ester transfer protein and lipoprotein lipase (LPL).
Main Results:
- Plasma apoC-II levels remained unchanged post-HD.
- Plasma apoC-III levels showed a slight decrease after HD.
- Significant reduction in plasma apoC-I, primarily from VLDL, was observed.
- Post-HD VLDL showed enhanced LPL substrate activity, but no change in CETP interaction.
Conclusions:
- Hemodialysis leads to a significant loss of apoC-I from VLDL.
- This loss may improve VLDL's ability to act as an LPL substrate.
- ApoC-I reduction during HD could be beneficial for triglyceride metabolism in renal patients.
Abstract:
Apolipoprotein Cs (apoC-1, apoC-II, and apoC-III) are lipoprotein components that have regulatory effects on enzymes involved in lipoprotein metabolism. Owing to their low molecular weights, apoCs can adsorb onto and/or pass through dialysis membranes. Our study determines the consequence of hemodialysis (HD) on plasma concentrations of apoCs and on the activities of enzymes modulated by apoCs. Plasma samples were collected from 28 patients with chronic renal failure before and after HD. Plasma apoC-II levels were unchanged, whereas apoC-III levels were slightly decreased in post-dialysis plasmas. The apoC-I content was markedly reduced during HD. This was due to a significant decrease in the apoC-I content of very low-density lipoprotein (VLDL), whereas the apoC-I content of high-density lipoprotein (HDL) was unchanged. Although HDL bound apoC-I is thought to inhibit cholesterol ester transfer protein, no change in the ability of pre- and post-dialysis VLDL to interact with the transfer protein were observed. Complementary experiments confirmed that VLDL-bound apoC-I has no transfer protein inhibitory potential. In contrast, an increase in the ability of post-dialysis apoC-I-poor VLDL to act as substrate for lipoprotein lipase (LPL) was found compared to pre-dialysis VLDL. Our study shows that apoC-I losses during HD might be beneficial by improving the ability of VLDL to be a substrate for LPL thus improving plasma triglyceride metabolism.
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