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  • Title: What are the biochemical mechanisms responsible for enhanced fatty acid utilization by perfused hearts from type 2 diabetic db/db mice?
    Author: Carley AN, Severson DL.
    Journal: Cardiovasc Drugs Ther; 2008 Apr; 22(2):83-9. PubMed ID: 18247111.
    Abstract:
    INTRODUCTION: It is generally accepted that diabetic hearts have an altered metabolic phenotype, with enhanced fatty acid (FA) utilization. The over-utilization of FA by diabetic hearts can have deleterious functional consequences, contributing to a distinct diabetic cardiomyopathy. The objective of this review will be to examine which biochemical mechanisms are responsible for enhanced FA utilization by diabetic hearts. METHODOLOGY AND RESULTS: Studies were performed with db/db mice, a monogenic model of type 2 diabetes with extreme obesity and hyperglycemia. Perfused db/db hearts exhibit enhanced FA oxidation and esterification. Hypothesis 1: Cardiac FA uptake is enhanced in db/db hearts. The plasma membrane content of two FA transporters, fatty acid translocase/CD36 (FAT/CD36) and plasma membrane fatty acid binding protein (FABPpm), was increased in db/db hearts, consistent with hypothesis 1. Hypothesis 2: Cardiac FA oxidation is enhanced in db/db hearts due to mitochondrial alterations. However, the activity of carnitine palmitoyl transferase-1 (CPT-1) and sensitivity to inhibition by malonyl CoA was unchanged in mitochondria from db/db hearts. Furthermore, total malonyl CoA content was increased, not decreased as predicted for elevated FA oxidation. Finally, the content of uncoupling protein-3 was unchanged in db/db heart mitochondria. CONCLUSION: Increased plasma membrane content of FA transporters (FAT/CD36 and FABPpm) will increase FA uptake into db/db cardiomyocytes and thus increase FA utilization. On the other hand, mitochondrial mechanisms do not contribute to elevated rates of FA oxidation in db/db hearts.
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