HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 288/6/E1120    most recent 00588.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (4) Citing Articles via Google Scholar Google Scholar Articles by An, D. Articles by Rodrigues, B. Search for Related Content PubMed PubMed Citation Articles by An, D. Articles by Rodrigues, B.

-Agonist stimulation produces changes in cardiac AMPK and coronary lumen LPL only during increased workload

¹Faculty of Pharmaceutical Sciences, Departments of ²Pathology and Laboratory Medicine and ³Pediatrics, The University of British Columbia, Vancouver, British Columbia, Canada

Submitted 13 December 2004 ; accepted in final form 27 January 2005

Given the importance of lipoprotein lipase (LPL) in cardiac and vascular pathology, the objective of the present study was to investigate whether the -agonist isoproterenol (Iso) influences cardiac LPL. Incubation of quiescent cardiomyocytes with Iso for 60 min had no effect on basal, intracellular, or heparin-releasable (HR)-LPL activity. Similarly, Iso did not change HR-LPL in Langendorff isolated hearts that do not beat against an afterload. In the intact animal, LPL activity at the vascular lumen increased significantly in the Iso-treated group, together with a substantial increase in rate-pressure product. This LPL increase was likely via mechanisms regulated by activation of AMP-activated protein kinase (AMPK) and inactivation of acetyl-CoA carboxylase (ACC₂₈₀). In glucose-perfused hearts, simply switching from Langendorff to the isolated working heart (that beats against an afterload) induced increases in AMPK and ACC₂₈₀ phosphorylation and enhanced HR-LPL activity. Provision of insulin and albumin-bound palmitic acid to the working heart was able to reverse these effects. In these hearts, introduction of Iso to the buffer perfusate duplicated the effects seen when this -agonist was given in vivo. Our data suggest that Iso can influence HR-LPL only during conditions of increased workload, mechanical performance and excessive energy expenditure, and likely in an AMPK-dependent manner.

isoproterenol; acetyl-coenzyme A carboxylase; cardiomyocyte; Langendorff heart; working heart; adenosine 3',5'-monophosphate-activated protein kinase; lipoprotein lipase

This article has been cited by other articles:

				L. Magnoni, E. Vaillancourt, and J.-M. Weber In vivo regulation of rainbow trout lipolysis by catecholamines J. Exp. Biol., August 1, 2008; 211(15): 2460 - 2466. [Abstract] [Full Text] [PDF]

				R. Saeedi, H. L. Parsons, R. B. Wambolt, K. Paulson, V. Sharma, J. R. B. Dyck, R. W. Brownsey, and M. F. Allard Metabolic actions of metformin in the heart can occur by AMPK-independent mechanisms Am J Physiol Heart Circ Physiol, June 1, 2008; 294(6): H2497 - H2506. [Abstract] [Full Text] [PDF]

				G. Wu, L. Zhang, J. Gupta, G. Olivecrona, and T. Olivecrona A transcription-dependent mechanism, akin to that in adipose tissue, modulates lipoprotein lipase activity in rat heart Am J Physiol Endocrinol Metab, October 1, 2007; 293(4): E908 - E915. [Abstract] [Full Text] [PDF]

				V. W. Dolinsky and J. R. B. Dyck Role of AMP-activated protein kinase in healthy and diseased hearts Am J Physiol Heart Circ Physiol, December 1, 2006; 291(6): H2557 - H2569. [Abstract] [Full Text] [PDF]