期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
卷 1781, 期 10, 页码 618-626出版社
ELSEVIER
DOI: 10.1016/j.bbalip.2008.07.006
关键词
Cardiac hypertrophy; Very-low-density lipoprotein receptor; AMPK; Triacylglycerol
资金
- British Heart Foundation [PC/06/007]
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 AMPK alpha 2 and phospho-AMPK alpha 2 were unaffected. These observations indicate that for physiological hyper-trophy AMPK phosphorylation does not mediate the enhanced translocation of LPL to cardiac endothelium. (c) 2008 Elsevier B. V. All rights reserved.
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