Abstract
Current evidence suggests the benefit of a diet containing anaplerotic odd‐chain medium chain fatty acid (MCFAs) for cardiac symptoms in patients with long chain fatty acid oxidation defects (Roe & coll. JCI, 110(2):259‐69, 2002), although the underlying mechanism remains unclear. We conducted a study to evaluate the anaplerotic status of VLCAD−/− mouse hearts, using our working mouse heart model and 13C‐methodology. Furthermore, the expression of selected anaplerotic genes (using real time PCR), and the myocardial levels of CAC intermediates were assessed in fed and 24h fasted mice. Compared to controls VLCAD+/+, 3 month‐old VLCAD−/− hearts showed a 40% lower anaplertoic flux through pyruvate carboxylation (p<0.05). Furthermore, VLCAD−/− hearts displayed lower mRNA levels for enzymes involved in anaplerosis, namely pyruvate and propionyl‐CoA carboxylase, but not malic enzyme, when compared to their normal counterparts, changes that were however age‐ and condition‐dependent. Besides, two‐way Anova revealed a species effect on CAC intermediates levels, specifically succinate and malate, which were lower in VLCAD−/− hearts from 7 month‐old mice. Collectively, our data highlight, impaired anaplerosis in VLCAD−/− mouse hearts, suggesting a potential beneficial role for odd‐chain MCFAs. (Supported by NIH & CIHR)
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