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The hepatic BMAL1/AKT/lipogenesis axis protects against alcoholic liver disease in mice via promoting PPARα pathway
Liver BMAL1/AKT pathway helps protect against alcoholic liver disease in mice by boosting fat metabolism through PPARα
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Abstract
The circadian clock protein BMAL1 is necessary and sufficient to protect mice from alcohol liver disease (ALD).
- Mice lacking BMAL1 in liver cells develop more severe liver fat accumulation and injury when fed an ethanol diet.
- The absence of BMAL1 leads to reduced formation of new fatty acids and impaired breakdown of fatty acids.
- Supplementation with synthetic PPARα ligands can reverse the effects of BMAL1 depletion on liver fat and injury.
- Activating the protein AKT in BMAL1-deficient mice increases fatty acid breakdown and reduces alcohol-induced liver damage.
- Over-expressing the transcription factor ChREBP in BMAL1-deficient mice enhances fatty acid oxidation and partially mitigates liver damage from ethanol.
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