Key result
Cardiac-specific overexpression of alcohol dehydrogenase exacerbated acute ethanol toxicity-induced myocardial contractile dysfunction and glucose intolerance, associated with hyperphosphorylated AMPK signaling.
Why the study?
Does cardiac-specific overexpression of alcohol dehydrogenase accentuate acute ethanol-induced myocardial dysfunction in mice?
Population
ADH transgenic and wild-type FVB mice
Comparison
Acute ethanol challenge for 3 days vs Wild-type FVB mice
Design
Preclinical
Follow-up
3 days
Authors
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Cardiac ADH overexpression worsens ethanol toxicity in mice; leaves open human relevance of AMPK pathway.
Does cardiac-specific overexpression of alcohol dehydrogenase accentuate acute ethanol-induced myocardial dysfunction in mice?
Cardiac-specific overexpression of alcohol dehydrogenase exacerbates acute ethanol-induced myocardial contractile dysfunction and calcium mishandling, likely via the AMPK signaling cascade.
Guo et al. (2010) studied Acute ethanol toxicity-induced myocardial dysfunction. Acute ethanol challenge vs. Wild-type FVB mice without ethanol was evaluated on Myocardial contractile dysfunction and AMPK signaling. Cardiac-specific overexpression of alcohol dehydrogenase exacerbated acute ethanol toxicity-induced myocardial contractile dysfunction and glucose intolerance, associated with hyperphosphorylated AMPK signaling.
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