Suppression of Hepatic Flotillin-1 by Type 2 Diabetes Impairs the Disposal of Remnant Lipoproteins via Syndecan-1

Objectives Type 2 diabetes mellitus (T2DM) and the atherometabolic syndrome exhibit a deadly dyslipoproteinemia that arises in part from impaired hepatic disposal of cholesterol- and triglyceride-rich remnant apoB-lipoproteins (C-TRLs). We previously identified syndecan-1 as a receptor for C-TRLs that directly mediates endocytosis via rafts, independent from coated pits. Caveolins and flotillins form rafts but facilitate distinct endocytotic pathways. We now investigated their participation in syndecan-1-mediated disposal of C-TRLs and their expression in T2DM liver.