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on July 18, 2002

Arteriosclerosis, Thrombosis, and Vascular Biology. 2002
Published online before print July 18, 2002, doi: 10.1161/01.ATV.0000030199.06252.26
A more recent version of this article appeared on September 1, 2002
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Submitted on April 22, 2002
Accepted on July 3, 2002

Microsomal Triglyceride Transfer Protein Gene Expression and Triglyceride Accumulation in Hypoxic Human Hearts

Lars B. Nielsen *; Mario Perko ; Henrik Arendrup ; and Claus B. Andersen

From the Department of Clinical Biochemistry (L.B.N.), Department of Thoracic Surgery (M.P., H.A.), and Department of Pathology (C.B.A.), Rigshospitalet, University of Copenhagen, Denmark.

* To whom correspondence should be addressed. E-mail: larsbo{at}rh.dk.

Objectives—Cardiac myocytes secrete apolipoprotein (apo)B-containing lipoproteins. Their function may be the removal of triglycerides when ß-oxidation of fatty acids is decreased, eg, during hypoxia. To test this hypothesis, we examined heart biopsies from patients undergoing coronary artery bypass graft (CABG, n=13) or valve replacement (n=6) surgery.

Methods and Results—Ventricular microsomal triglyceride transfer protein (P=0.02) and apoB (P=0.04) mRNA levels were both {approx}2-fold higher in CABG compared with valve replacement patients. In CABG patients, ventricular microsomal triglyceride transfer protein mRNA levels were negatively associated with the triglyceride content in ventricular myocytes (r=-0.70; P=0.02) and with mRNA levels of sterol regulatory element binding protein-1 (r=-0.74; P=0.004).

Conclusions—The results are compatible with the notion that cardiac lipoprotein production is increased in hypoxic human ventricle, possibly as a result of decreased sterol regulatory element binding protein-1 expression. This might attenuate accumulation of triglycerides in cardiac myocytes.


Key words: hypoxia • lipids • lipoproteins • myocytes




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