Rafting for gallstones by slowing mass transit

摘要

Much has been learned about the predisposing factors that contribute to cholesterol gallstone disease and we now have a more granular understanding of the pathways that promote cholesterol monohydrate crystal formation and in turn lead to the formation of cholesterol gallstones. There are several sets of players involved, some of which have been invoked from studies using inbred lines of mice with differing susceptibility to map quantitative trait loci (QTLs) (Lyons & Wittenburg, 2006), while others have been inferred from gain- and loss-of-function approaches based on candidate genes (for example ABCG5/G8) identified through biochemical and molecular screens (Krawczyk et al. 2011). The emerging sense from these various approaches is that a range of genetic and acquired defects in intestinal, hepatic, canalicular and gallbladder signalling pathways can lead to the production of supersaturated bile. By comparison, there is a paucity of information regarding the influence of enterohepatic cholesterol cycling on intestinal motility and its possible contribution to gallstone susceptibility.