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High-density lipoprotein delivered after myocardial infarction increases cardiac glucose uptake and function in mice

Citation

Heywood, SE and Richart, AL and Henstridge, DC and Alt, K and Kiriazis, H and Zammit, C and Carey, AL and Kammoun, HL and Delbridge, LM and Reddy, M and Chen, Y-C and Du, X-J and Hagemeyer, CE and Febbraio, MA and Siebel, AL and Kingwell, BA, High-density lipoprotein delivered after myocardial infarction increases cardiac glucose uptake and function in mice, Science Translational Medicine, 9, (411) pp. eaam6084. ISSN 1946-6234 (2017) [Refereed Article]

Copyright Statement

Copyright 2017 The Authors

DOI: doi:10.1126/scitranslmed.aam6084

Abstract

Protecting the heart after an acute coronary syndrome is a key therapeutic goal to support cardiac recovery and prevent progression to heart failure. A potential strategy is to target cardiac glucose metabolism at the early stages after ischemia when glycolysis is critical for myocyte survival. Building on our discovery that high-density lipoprotein (HDL) modulates skeletal muscle glucose metabolism, we now demonstrate that a single dose of reconstituted HDL (rHDL) delivered after myocardial ischemia increases cardiac glucose uptake, reduces infarct size, and improves cardiac remodeling in association with enhanced functional recovery in mice. These findings applied equally to metabolically normal and insulin-resistant mice. We further establish direct effects of HDL on cardiomyocyte glucose uptake, glycolysis, and glucose oxidation via the Akt signaling pathway within 15 min of reperfusion. These data support the use of infusible HDL preparations for management of acute coronary syndromes in the setting of primary percutaneous interventions.

Item Details

Item Type:Refereed Article
Keywords:glucose, high density lipoprotein, reconstituted high density lipoprotein, unclassified drug, glucose, high density lipoprotein, Akt signaling, animal cell, animal experiment, animal model, animal tissue, capillary density, controlled study
Research Division:Biological Sciences
Research Group:Biochemistry and cell biology
Research Field:Cell metabolism
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Henstridge, DC (Mr Darren Henstridge)
ID Code:133373
Year Published:2017
Web of Science® Times Cited:31
Deposited By:Health Sciences
Deposited On:2019-06-24
Last Modified:2019-07-31
Downloads:0

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