OBJECTIVES: Cardiac myocytes secrete apolipoprotein (apo)B-containing lipoproteins. Their function may be the removal of triglycerides when beta-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 approximately 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.
OBJECTIVES: Cardiac myocytes secrete apolipoprotein (apo)B-containing lipoproteins. Their function may be the removal of triglycerides when beta-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 approximately 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 hypoxichuman ventricle, possibly as a result of decreased sterol regulatory element binding protein-1 expression. This might attenuate accumulation of triglycerides in cardiac myocytes.
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