Ischemia-reperfusion alters cardiac lipoprotein lipase

Biochim Biophys Acta. 2010 Feb;1801(2):171-5. doi: 10.1016/j.bbalip.2009.10.008. Epub 2009 Oct 24.

Abstract

Ischemia-reperfusion (I/R) is associated with changes in energy metabolism in the heart. However, the majority of studies have focused on examining rates and extent of fatty acid (FA) oxidation, with limited emphasis on FA delivery. We examined the influence of acute myocardial I/R on coronary lipoprotein lipase (LPL), the key enzyme responsible for triglyceride-lipoprotein hydrolysis and FA delivery to the heart. In a whole animal and an ex vivo model of I/R, we demonstrate increases in luminal LPL activity, an effect that involved signaling through nitric oxide. Given the damaging effect of excess FA utilization by the ischemic heart, strategies to restrict LPL at the vascular lumen would be an attractive therapeutic option in limiting I/R related cardiac injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Fatty Acids / metabolism
  • Heart / physiology*
  • Ischemia / enzymology*
  • Lipoprotein Lipase / metabolism*
  • Lipoproteins / metabolism
  • Male
  • Myocardial Reperfusion*
  • Myocytes, Cardiac / enzymology*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type II / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Oxygen Consumption
  • Rats
  • Rats, Wistar
  • Triglycerides / metabolism

Substances

  • Fatty Acids
  • Lipoproteins
  • Triglycerides
  • lipoprotein triglyceride
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos2 protein, rat
  • Nos3 protein, rat
  • Lipoprotein Lipase