Journal article
Genetic manipulation of cardiac Hsp72 levels does not alter substrate metabolism but reveals insights into high-fat feeding-induced cardiac insulin resistance
DC Henstridge, E Estevez, TL Allen, SE Heywood, T Gardner, C Yang, NA Mellett, BA Kingwell, PJ Meikle, MA Febbraio
Cell Stress and Chaperones | SPRINGER | Published : 2015
Abstract
Heat shock protein 72 (Hsp72) protects cells against a variety of stressors, and multiple studies have suggested that Hsp72 plays a cardioprotective role. As skeletal muscle Hsp72 overexpression can protect against high-fat diet (HFD)-induced insulin resistance, alterations in substrate metabolism may be a mechanism by which Hsp72 is cardioprotective. We investigated the impact of transgenically overexpressing (Hsp72 Tg) or deleting Hsp72 (Hsp72 KO) on various aspects of cardiac metabolism. Mice were fed a normal chow (NC) or HFD for 12 weeks from 8 weeks of age to examine the impact of diet-induced obesity on metabolic parameters in the heart. The HFD resulted in an increase in cardiac fatt..
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Awarded by State Government of Victoria
Funding Acknowledgements
We wish to acknowledge Deb Ramsey and her team at the AMREP AS for their assistance with the animal studies, Jacqui Weir for technical assistance, and Helene Kammoun for critically reviewing the manuscript. This study was supported by grants from the National Health and Medical Research Council of Australia (NHMRC Project Grant 1004441) and the Victorian Government Operational Infrastructure Support Program. MAF and BAK (1059454) are Senior Principal Research Fellows of the NHMRC. PJM is a Senior Research Fellow of the NHMRC. DCH is supported by a National Heart Foundation (NHF) Biomedical Postdoctoral Fellowship and an Australian Diabetes Society (ADS) Skip Martin Fellowship. The original Hsp72 Tg mouse line was provided by Prof Ruben Mestril.