Genetic background of cholesterol gallstone disease.

Cholesterol gallstone formation is a multifactorial process involving a multitude of metabolic pathways. The primary pathogenic factor is hypersecretion of free cholesterol into bile. For people living in the Western Hemisphere, this is almost a normal condition, certainly in the elderly, which explains the very high incidence of gallstone disease.

Understanding and controlling hepatobiliary function.

Over the past decade, enormous progress has been made in identifying the mechanisms that underlie hepatobiliary excretion. A set of transport proteins mediates the canalicular transport of most important bile constituents. With the discovery of these transporter genes, the mechanism of bile formation could be partly elucidated and genetic defects caused by mutations in these genes identified.

Adenoviral overexpression of apolipoprotein A-V reduces serum levels of triglycerides and cholesterol in mice.

Mice lacking ApoA-V, a novel HDL-associated apolipoprotein identified by our group and independently by Pennacchio et al. [Science 294 (2001) 169], were recently shown to be hypertriglyceridemic. To study the role of ApoA-V in triglyceride homeostasis, we compared lipid profiles in mice expressing normal and highly elevated levels of ApoA-V.