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This Article Full Text Full Text (PDF) All Versions of this Article: 295/3/E705    most recent 90338.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Yamashita, H. Articles by Goldberg, I. J. PubMed PubMed Citation Articles by Yamashita, H. Articles by Goldberg, I. J.

Cardiac metabolic compensation to hypertension requires lipoprotein lipase

¹Divisions of Preventive Medicine and Nutrition, and Cardiology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York; ²Department of Medicine, Lee Gil Ya Cancer and Diabetes Institute, and Gachon University, Incheon, Korea

Submitted 5 April 2008 ; accepted in final form 10 July 2008

Fatty acids (FAs) are acquired from free FA associated with albumin and lipoprotein triglyceride that is hydrolyzed by lipoprotein lipase (LpL). Hypertrophied hearts shift their substrate usage pattern to more glucose and less FA. However, FAs may still be an important source of energy in hypertrophied hearts. The aim of this study was to examine the importance of LpL-derived FAs in hypertensive hypertrophied hearts. We followed cardiac function and metabolic changes during 2 wk of angiotensin II (ANG II)-induced hypertension in control and heart-specific lipoprotein lipase knockout (hLpL0) mice. Glucose metabolism was increased in ANG II-treated control (control/ANG II) hearts, raising it to the same level as hLpL0 hearts. FA uptake-related genes, CD36 and FATP1, were reduced in control/ANG II hearts to levels found in hLpL0 hearts. ANG II did not alter these metabolic genes in hLpL0 mice. LpL activity was preserved, and mitochondrial FA oxidation-related genes were not altered in control/ANG II hearts. In control/ANG II hearts, triglyceride stores were consumed and reached the same levels as in hLpL0/ANG II hearts. Intracellular ATP content was reduced only in hLpL0/ANG II hearts. Both ANG II and deoxycorticosterone acetate-salt induced hypertension caused heart failure only in hLpL0 mice. Our data suggest that LpL activity is required for normal cardiac metabolic compensation to hypertensive stress.

hypertrophy; heart failure; fatty acids; triglyceride; angiotensin II; deoxycorticosterone acetate