The Durk Pearson & Sandy Shaw®
Life Extension NewsTM
Volume 18 No. 8 • December 2015

Lipolysis May Mediate the Proinflammatory Effects of Very Low Density Lipoprotein (VLDL)

In a 2006 paper (Saraswathi and Hasty, 2006), researchers studied the effect of incubating mouse peritoneal macrophages with 100 μg/ml VLDL for six hours, finding that it resulted in 2.8 to 3.7 fold increases in intracellular triglycerides and free fatty acids, respectively, via intracellular hydrolysis (lipolysis). There were significant increases of at least two fold in inflammatory proteins as well, including TNFalpha, IL-1beta, MCP-1 (monocyte chemoattractant protein-1, intercellular adhesion molecule 1, matrix metalloproteinase 3 (MMP3), and macrophage inflammatory protein 1alpha. The authors suggest that these changes point to a direct proatherogenic effect of VLDL. The increases in triglycerides and free fatty acids was eliminated by Orlistat, an OTC weight-loss drug.

Interestingly, VLDL is known to be the lipoprotein carrier for apoE4. “ApoE3 binds preferentially to HDL and apoE4 to VLDL.” (Tetali, 2010). The fact that the ApoE4 gene is being carried by a potentially proinflammatory lipoprotein suggests the possibility of an interplay that may increase the adverse effects of apoE4. Suggestion: keep your VLDL level down. Niacin is very effective at this, as is fish oils.


  • Saraswathi and Hasty. The role of lipolysis in mediating the proinflammatory effects of very low density lipoproteins in mouse peritonial macrophages. J Lipid Res. 47:1406-16 (2006).
  • Tetali, Budamagunta, Simion, et al. VLDL lipolysis products increase VLDL fluidity and convert apolipoprotein E4 into a more expanded conformation. J Lipid Res. 51:1273-83 (2010).

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