Ischemia-reperfusion alters cardiac lipoprotein lipase

Thomas Pulinilkunnil; Prasanth Puthanveetil; Min Suk Kim; Fang Wang; Veronika Schmitt; Brian Rodrigues

doi:10.1016/j.bbalip.2009.10.008

Ischemia-reperfusion alters cardiac lipoprotein lipase

Thomas Pulinilkunnil, Prasanth Puthanveetil, Min Suk Kim, Fang Wang, Veronika Schmitt, Brian Rodrigues

Research output: Contribution to journal › Article › peer-review

10 Citations (Scopus)

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.

Original language	English
Pages (from-to)	171-175
Number of pages	5
Journal	Biochimica et Biophysica Acta - Molecular and Cell Biology of Lipids
Volume	1801
Issue number	2
DOIs	https://doi.org/10.1016/j.bbalip.2009.10.008
Publication status	Published - Feb 2010
Externally published	Yes

ASJC Scopus Subject Areas

Molecular Biology
Cell Biology

PubMed: MeSH publication types

Journal Article
Research Support, Non-U.S. Gov't

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10.1016/j.bbalip.2009.10.008

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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.",

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AU - Pulinilkunnil, Thomas

AU - Puthanveetil, Prasanth

AU - Kim, Min Suk

AU - Wang, Fang

AU - Schmitt, Veronika

AU - Rodrigues, Brian

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Ischemia-reperfusion alters cardiac lipoprotein lipase

Abstract

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