Heparanase Shakes HandsWith Lipoprotein Lipase: A Tale of Two

Altered metabolism with excess provision of lipid sub-strates may be a major pathogenetic factor linking di-abetes with cardiovascular disease—lipoprotein lipase (LPL) being one facilitator of such a process (1,2). Hyper-lipidemia, by itself, plays a major role in lipid-provoked cardiovascular pathologies, largely mediated through LPL (3). Under physiological state, due to their presence on the endothelial cell surface, LPLs break down triglyceride lipoproteins in the circulation and provide tissues, like heart and skeletal muscle, with the required fatty acid substrates to derive ATP (3,4). A large volume of data, using genetically manipulated animal models and clinical studies, has found that LPL homeostasis is required for normal cardiac metabolism and function (5,6). In diabe-tes, increased metabolic demand of the heart is met b