Numerous studies using a variety of cell/acceptor combinations have demonst
rated differences in cholesterol efflux among cells. These studies also sho
w that different accepters, ranging from simple molecules like cyclodextrin
s to serum, stimulate efflux through a variety of mechanisms. By combining
early observations with data derived from recent studies, it is now possibl
e to formulate a model for cell cholesterol efflux which proposes that an a
rray of different mechanisms, including aqueous diffusion, lipid-free apoli
poprotein membrane microsolubilization, and SR-BI-mediated cholesterol exch
ange contribute to cholesterol flux. In this model the relative importance
of each mechanism would be determined both by the cell type and the nature
of the extracellular cholesterol acceptor.