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Very Low Density Lipoproteins Promote Triglyceride Accumulation in Macrophages

Very Low Density Lipoproteins Promote Triglyceride Accumulation in Macrophages Incubation of mouse peritoneal macrophages with very low density lipoproteins (VLDL) from normal rats or rhesus monkeys markedly increased the levels of intracellular trlglycerldes by 10-to 56-fold and was accompanied by the production of oil red 0 positive vacuoles. The stimulation of triglyceride accumulation in macrophages was timeand concentration-dependent and was specific for VLDL. Three possible mechanisms for the VLDL-stlmulated triglyceride accumulation In macrophages were explored: receptor-mediated uptake, action of llpoprotein llpase, and phagocytosis. Macrophage uptake and degradation of 125I-monkey and rat VLDL demonstrated saturable and nonsaturable components. Uptake of 125I-VLDL could be inhibited by unlabeled normal VLDL, although hyperllpemlc VLDL was more effective. HDL did not compete to a significant extent. Heparln released llpoprotein lipase-llke activity from peritoneal macrophages. Addition of heparln with VLDL resulted in a greater, more rapid elevation in Intracellular triglycerides, which was partially Inhibited by albumin. Free fatty acid and Intrallpid also produced triglyceride accumulation In macrophages. The data showed that all three of the mechanisms examined could contribute to the metabolism of VLDL by macrophages and cause the production of trlglycerlderlch cells with a “foamy” appearance, although the evidence suggested that the action of llpoprotein llpase was probably the most important In this process. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Very Low Density Lipoproteins Promote Triglyceride Accumulation in Macrophages

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Copyright
© 1984 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Incubation of mouse peritoneal macrophages with very low density lipoproteins (VLDL) from normal rats or rhesus monkeys markedly increased the levels of intracellular trlglycerldes by 10-to 56-fold and was accompanied by the production of oil red 0 positive vacuoles. The stimulation of triglyceride accumulation in macrophages was timeand concentration-dependent and was specific for VLDL. Three possible mechanisms for the VLDL-stlmulated triglyceride accumulation In macrophages were explored: receptor-mediated uptake, action of llpoprotein llpase, and phagocytosis. Macrophage uptake and degradation of 125I-monkey and rat VLDL demonstrated saturable and nonsaturable components. Uptake of 125I-VLDL could be inhibited by unlabeled normal VLDL, although hyperllpemlc VLDL was more effective. HDL did not compete to a significant extent. Heparln released llpoprotein lipase-llke activity from peritoneal macrophages. Addition of heparln with VLDL resulted in a greater, more rapid elevation in Intracellular triglycerides, which was partially Inhibited by albumin. Free fatty acid and Intrallpid also produced triglyceride accumulation In macrophages. The data showed that all three of the mechanisms examined could contribute to the metabolism of VLDL by macrophages and cause the production of trlglycerlderlch cells with a “foamy” appearance, although the evidence suggested that the action of llpoprotein llpase was probably the most important In this process.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Mar 1, 1984

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