Figure 1.

Regulatory processes that influence cardiac lipoprotein lipase action and the utilization of delivered FAs. Following its synthesis and activation in cardiomyocytes (1), the actin cytoskeleton traffics LPL to myocyte cell surface HSPG under the control of AMPK (2). Onward progress is facilitated by heparanase (Hpa) secreted from the endothelial cell that cleaves HSPG side chains to liberate LPL (3). GPIHBP1 captures this interstitial LPL and relocates it from the basolateral to the apical side of endothelial cell (4). At this location, a GPIHBP1 platform and LPL enables lipoprotein-TG hydrolysis to generate FAs (5) that are delivered to the cardiomyocyte (6). In the cardiomyocyte, FAs have two major fates (7). They can either undergo mitochondrial beta-oxidation and oxidative phosphorylation to generate ATP (8) or accumulate as lipid metabolites/droplets (9). Lipid intermediates are known to effect insulin signaling and substrate utilization. LPC: lysophosphatidylcholine; DAG: diacylglycerol.