The ABCG5 ABCG8 (G5G8) sterol transporter opposes the accumulation of dietary xenosterols, but is also the primary mediator of biliary cholesterol secretion in the cholesterol elimination pathway. In humans and in mouse models of disrupted biliary cholesterol secretion, fecal neutral sterols remain constant, indicating the presence of a G5G8-independent mechanism for cholesterol excretion. Transintestinal cholesterol elimination (TICE) is thought to compensate for biliary G5G8 insufficiency. We sought to measure the compensatory increase in intestinal cholesterol secretion and provide mechanistic insight for how TICE maintains sterol balance in the absence of G5G8. Differences were not observed in fecal neutral sterols between control, acute, and chronic liver-specific G5G8 deficient mice (G5G8