Prior studies suggesting that ApoC - III may predominantly affect LPL - mediated
TG hydrolysis were based on fractional clearance rates of ApoB in patients lacking ApoC - III and ApoA - I (13) and in vitro studies showing that excess ApoC - III (or ApoC - I) blocks LPL activity in lipid droplets or emulsions possibly due to competition for the lipid - water interface (12, 19).
At these levels, the residual activity could be due to other lipases that cross-react in
the TG hydrolysis assay (e.g., hepatic lipase, hormone - sensitive lipase, or adipose TG lipase).