ABCG5/ABCG8-independent mechanisms fail to maintain sterol balance in mice fed a high-cholesterol diet.

ABSTRACT: The ABCG5/ABCG8 (G5G8) sterol transporter opposes the accumulation of dietary xenosterols but is also the primary mediator of biliary cholesterol secretion. In humans and in mouse models of disrupted biliary cholesterol secretion, fecal neutral sterols (FNSs) remain constant, indicating the presence of an alternate pathway for cholesterol excretion. Transintestinal cholesterol elimination or excretion (TICE) is thought to compensate for biliary disruptions and 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 hepatic G5G8. Differences were not observed in FNSs between control, acute, and chronic liver-specific G5G8-deficient mice (G5G8^LKO).

SUBMITTER: Anspach GB 

PROVIDER: S-EPMC12550799 | biostudies-literature | 2025 Sep

REPOSITORIES: biostudies-literature