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1 Division of Endocrinology and 2 Department of Psychiatry, Stanford University, Stanford 94305; 3 Mental Illness Research, Education, and Clinical Center, and 4 Geriatric Research, Education and Clinical Center, Veterans Affairs Palo Alto Health Care System, Palo Alto, California 94304; and 5 Department of Biochemistry, University of Nijmegen, 6500 HB Nijmegen, The Netherlands
Hormone-sensitive lipase
(HSL) hydrolyzes triglyceride (TG) in adipose tissue. HSL is also
expressed in heart. To explore the actions of cardiac HSL,
heart-specific, tetracycline (Tc)-controlled HSL-overexpressing mice
were generated. Tc-responsive element-HSL transgenic (Tg) mice were
generated and crossed with myosin heavy chain (MHC)
-tTA Tg mice,
which express the Tc-responsive transactivator (tTA) in the heart. The
double-Tg mice (MHC-HSL) were maintained with doxycycline (Dox) to
suppress Tg HSL. Upon removal of Dox, cardiac HSL activity and protein
increased 12- and 8-fold, respectively, and the expression was heart
specific. Although cardiac TG content increased twofold in control mice
after an overnight fast, it did not increase in HSL-induced mice.
Electron microscopy showed numerous lipid droplets in the myocardium of
fasted control mice, whereas fasted HSL-induced mice showed virtually
no droplets. Microarray analysis showed altered expression of cardiac
genes for fatty acid oxidation, transcription factors, signaling
molecules, cytoskeletal proteins, and histocompatibility antigens in
HSL-induced mice. Thus cardiac HSL plays a role in controlling
accumulation of triglyceride droplets and can affect the expression of
a number of cardiac genes.
hormone-sensitive lipase; gene expression; microarray analysis
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