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Updated: Jul 23, 2025

Measuring the Rate of Lipolysis in Ex Vivo Murine Adipose Tissue and Primary Preadipocytes Differentiated In Vitro
Published on: March 17, 2023
Triglyceride-Rich Lipoprotein Metabolism: Key Regulators of Their Flux
1Glycation, Oxidation and Disease Laboratory, Department of Research, Touro University California, Vallejo, CA 94592, USA.
Residual cardiovascular risk stems from lipid and immune issues. Triglyceride-rich lipoprotein (TRL) remnants are key contributors, driving atherogenesis despite statin therapy.
Area of Science:
- Cardiovascular Medicine
- Lipid Metabolism
- Atherosclerosis Research
Background:
- Optimal statin therapy leaves a significant residual risk (up to 50%) for arteriosclerotic cardiovascular disease.
- This residual risk is linked to both immunological factors and lipid disturbances, particularly triglyceride-rich lipoproteins (TRLs).
Purpose of the Study:
- To review the metabolism of TRLs and their remnants.
- To highlight the role of apolipoproteins, lipoprotein lipase, and their regulators in TRL metabolism.
- To discuss the impact of TRL remnants on atherogenesis and current therapeutic strategies.
Main Methods:
- Narrative review of TRL metabolism pathways.
- Summary of apolipoprotein functions and lipoprotein lipase regulation.
- Analysis of TRL fluxes in post-prandial states and their catabolism.
Main Results:
- TRLs and their remnants, rich in cholesterol, accumulate due to ineffective triglyceride catabolism and contribute to atherogenesis.
- Apolipoproteins, angiopoietin-like proteins, and apo CIII play crucial roles in TRL partitioning during metabolic cycles.
- Current therapeutic options and trial outcomes for managing TRL remnants are summarized.
Conclusions:
- TRL remnants represent a significant, modifiable target for reducing residual cardiovascular risk.
- Further research is needed to establish a gold standard for measuring TRL remnants.
- Understanding TRL metabolism is critical for developing novel atherogenesis therapies.
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