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. Author manuscript; available in PMC: 2013 Oct 19.
Published in final edited form as: Biochem Biophys Res Commun. 2012 Sep 18;427(2):361–365. doi: 10.1016/j.bbrc.2012.09.065

Figure 4. Model depicting the effect of apoA-V on the fate of hepatic TG.

Figure 4

In the absence of apoA-V (Upper Panel) TG accretion forms a lens between leaflets of the ER membrane. Expansion of this lens by continued accrual of TG leads to budding of a nascent lipid droplet from the cytoplasmic leaflet (left) or, alternatively, budding from the lumenal leaflet (right) to create a lumenal lipid droplet for utilization in VLDL maturation. Lower Panel) When present, apoA-V binding to membrane defects created by TG accumulation stabilizes the lumenal leaflet, promoting nascent lipid droplet budding toward the cytosol at the expense of lumenal lipid droplet formation (see arrows).