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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Curr Opin Lipidol. 2016 Feb;27(1):19–25. doi: 10.1097/MOL.0000000000000260

Figure 1. Hypothetical model for regulation of adipose inflammation by dietary cholesterol.

Figure 1

A. Dietary cholesterol enters the blood circulation in chylomicron particles. CM triglyceride is hydrolyzed to free fatty acids by lipoprotein lipase, resulting in CM remnant particles, FA uptake, and re-esterification into TG that is stored in the adipocyte lipid droplet. CMR, which are enriched with dietary cholesterol, bind to VLDL receptors expressed on the adipocyte plasma membrane through apolipoprotein E and are internalized, leading to a simultaneous increase in TG and free cholesterol content as adipocytes hypertrophy. During adipocyte hypertrophy, FC redistributes from the plasma membrane to the LD monolayer, resulting in a relative depletion of plasma membrane FC, which leads to adipocyte dysfunction, increased adipose tissue inflammation, and decreased insulin sensitivity. Optimal plasma membrane sphingomyelin content, maintained by ABCG1, appears necessary to maintain lipoprotein lipase activity for CM TG hydrolysis and adipocyte FA uptake. B. When adipocyte size decreases during LD TG hydrolysis to FA, adipocyte FC content is decreased via FC efflux to apoA-I, mediated by ABCA1, and to HDL, mediated by SRBI and probably by ABCG1, helping maintain a relativity constant FC:TG ratio for optimal adipocyte function. Thus, as adipocyte size and TG content is reduced, FC from the lipid droplet redistributes to the plasma membrane, restoring insulin sensitivity and reducing adipose tissue inflammation. Adipocyte phospholipid transfer protein activity may also be necessary for optimal FC efflux and nascent HDL particle formation. ABCA1, ATP binding cassette transporter A1; CM, chylomicron; CMR, chylomicron remnants; FA, free fatty acid; FC, free cholesterol; HDL, high-density lipoprotein; LD, lipid droplet; LPL, lipoprotein lipase; mϕ, macrophage; nHDL, nascent HDL; PLTP, phospholipid transfer protein; SM, sphingomyelin; SRBI, scavenger receptor class B, member 1; TG, triglyceride; VLDLR, very low-density lipoprotein receptor.