Key result
Fasted LCAD KO mice exhibited 2.7-fold higher myocardial PDH activity compared with fasted WT mice, reflecting an elevated reliance on glucose oxidation and impaired energy status.
Authors
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Highlights potential fasting vulnerability in LCAD deficiency; leaves open PDH modulation as therapeutic target in human fatty acid oxidation disorders.
Effect estimate: 2.7-fold higher
Bakermans et al. (2013) studied Mitochondrial long-chain fatty acid β-oxidation deficiency. Long-chain acyl-CoA dehydrogenase knockout (LCAD KO) vs. Wild-type (WT) mice was evaluated on In vivo pyruvate dehydrogenase (PDH) activity after fasting (2.7-fold higher). Fasted LCAD KO mice exhibited 2.7-fold higher myocardial PDH activity compared with fasted WT mice, reflecting an elevated reliance on glucose oxidation and impaired energy status.
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