Palmitoyl lysophosphatidylcholine mediated mobilization of LPL to the coronary luminal surface requires PKC activation.

Following diazoxide (DZ) induced hypoinsulinemia, cardiac luminal lipoprotein lipase (LPL) increases [Cardiovasc. Res. 3 (2003) 788].

Circulating triglyceride lipolysis facilitates lipoprotein lipase translocation from cardiomyocyte to myocardial endothelial lining.

Objective: Lipoprotein lipase (LPL) mediated hydrolysis of circulating triglyceride (TG)-rich lipoproteins provides the heart with fatty acids. The present study was designed to investigate the influence of circulating TG and their lipolysis in facilitating translocation of LPL from the underlying cardiomyocyte cell surface to the coronary lumen.

Methods: The in vivo effects of diazoxide (DZ), an agent that causes rapid hypoinsulinemia, and the in vitro effect of the lipoprotein breakdown product L-alpha-lysophosphatidylcholine (Lyso-PC) on luminal LPL were examined in Wistar rats.