Cheng_2008_Biochim.Biophys.Acta_1781_618

The contribution of triacylglycerol to energy provision in the hypertrophied heart, mediated through lipoprotein lipase (LPL) is largely unknown and the contribution of very-low-density lipoprotein (VLDL) receptor to control of LPL presentation at the endothelium is unclear. For isolated perfused rat hearts, cold acclimation (CA) induced volume-overload hypertrophy, with decreased developed pressure (P<0.01), increased end-diastolic volume of the left ventricle (P<0.001) and a loss of contractile reserve in response to dobutamine challenge (P<0.01). Oleate utilisation by perfused hearts was unchanged by CA, however uptake of intralipid emulsion increased 3-fold (P<0.01). CA increased the proportion of lipid deposited in tissue lipids from 10% in euthermic controls to 40% (P<0.01) although the overall contribution of individual lipid classes was unaffected. Cold acclimation significantly increased heparin-releasable LPL (P<0.05) and tissue residual LPL (P<0.01). Western blot analysis indicated preserved expression of proteins coding for SERCA2, muscle-CPT1 and VLDL-receptor following CA, while AMPKalpha2 and phospho-AMPKalpha2 were unaffected. These observations indicate that for physiological hypertrophy AMPK phosphorylation does not mediate the enhanced translocation of LPL to cardiac endothelium.