Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2001-9-11
pubmed:abstractText
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)alpha-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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0193-1849
pubmed:author
pubmed:issnType
Print
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
E857-66
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11551864-Animals, pubmed-meshheading:11551864-Crosses, Genetic, pubmed-meshheading:11551864-DNA Primers, pubmed-meshheading:11551864-Doxycycline, pubmed-meshheading:11551864-Eating, pubmed-meshheading:11551864-Enzyme Induction, pubmed-meshheading:11551864-Fasting, pubmed-meshheading:11551864-Gene Expression Regulation, Enzymologic, pubmed-meshheading:11551864-Genotype, pubmed-meshheading:11551864-Heart Ventricles, pubmed-meshheading:11551864-Lipid Metabolism, pubmed-meshheading:11551864-Lipids, pubmed-meshheading:11551864-Liver, pubmed-meshheading:11551864-Lung, pubmed-meshheading:11551864-Male, pubmed-meshheading:11551864-Mice, pubmed-meshheading:11551864-Mice, Transgenic, pubmed-meshheading:11551864-Muscle, Skeletal, pubmed-meshheading:11551864-Myocardium, pubmed-meshheading:11551864-Myosin Heavy Chains, pubmed-meshheading:11551864-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:11551864-Organ Specificity, pubmed-meshheading:11551864-Polymerase Chain Reaction, pubmed-meshheading:11551864-Rats, pubmed-meshheading:11551864-Recombinant Fusion Proteins, pubmed-meshheading:11551864-Spleen, pubmed-meshheading:11551864-Sterol Esterase, pubmed-meshheading:11551864-Testis, pubmed-meshheading:11551864-Trans-Activators
pubmed:year
2001
pubmed:articleTitle
Absence of cardiac lipid accumulation in transgenic mice with heart-specific HSL overexpression.
pubmed:affiliation
Division of Endocrinology, Stanford University, Stanford 94305, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't