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1 Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, The University of British Columbia, Vancouver, BC, Canada
* To whom correspondence should be addressed. E-mail: rodrigue{at}interchange.ubc.ca.
The "fuel gauge" AMP activated protein kinase (AMPK) facilitates ATP production to meet energy demands during metabolic stress. Given the importance of lipoprotein lipase (LPL) in providing hearts with fatty acids (FA), the preferred substrate consumed by the heart, the objective of the present study was to investigate if activation of AMPK influences LPL at its functionally relevant location, the coronary lumen. Hearts from overnight fasted rats were first perfused with heparin to release LPL, and homogenates from these hearts then used to measure total and phospho-AMPK-
by Western blotting. Manipulation of AMPK activity [with drugs like Ara-A and insulin (that inhibit) or perhexiline and oligomycin (that stimulate)] and its influence on LPL was also determined. Fasting augmented the activity of both AMPK and luminal LPL on immediate removal of hearts, effects that still remained even following in vitro perfusion of hearts for 1 hour. Inhibition of AMPK in fasted hearts using an inhibitor like Ara-A or through provision of insulin markedly lowered the enhanced luminal LPL activity. In contrast, AMPK activators like perhexiline and oligomycin produced a significant elevation in heparin-releasable LPL activity. Thus, using fasting or drugs that influence AMPK, a strong correlation between this metabolic switch and cardiac LPL activity was established. Our data suggest that in addition to its direct role in promoting FA oxidation, AMPK-mediated recruitment of LPL to the coronary lumen could represent an immediate compensatory response by the heart to guarantee FA supply.
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