title: Cold acclimation induces physiological cardiac hypertrophy and increases assimilation of triacylglycerol metabolism through lipoprotein lipase.
abstract: 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.
authors: Department of Physiology, Division of Medical Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, UK.
authors: Y
authors: Y
authors: Cheng
authors: D
authors: D
authors: Hauton
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000064:Acclimatization / Q000502:physiology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D006332:Cardiomegaly / Q000378:metabolism*; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D003080:Cold Temperature; D004075:Diglycerides / Q000378:metabolism; D004280:Dobutamine / Q000494:pharmacology; D005217:Fat Emulsions, Intravenous / Q000378:metabolism; D006321:Heart / Q000033:anatomy & histology / Q000187:drug effects / Q000502:physiology; D008071:Lipoprotein Lipase / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D019301:Oleic Acid / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D010084:Oxidation-Reduction; D010477:Perfusion; D051381:Rats; D017208:Rats, Wistar; D011973:Receptors, LDL / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism*
chemical_list: C506948:Atp2a2 protein, rat; D002788:Cholesterol Esters; D004075:Diglycerides; D005217:Fat Emulsions, Intravenous; D011973:Receptors, LDL; D014280:Triglycerides; C036053:VLDL receptor; D019301:Oleic Acid; D004280:Dobutamine; D002334:Carnitine O-Palmitoyltransferase; D055372:AMP-Activated Protein Kinases; D008071:Lipoprotein Lipase; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases