Do brain transcriptional responses to high-fat diet in Acads-deficient mice reveal energy sensing pathways?
Our results suggest that the decreased beta-oxidation of short-chain fatty acids in Acads-deficient mice fed HF diet produces a state of energy deficiency in the brain and that AMP-kinase may be the cellular energy-sensing mechanism linking fatty acid oxidation to feeding behavior in this model.
Among at-risk drinkers, persons with ARHE are a special subgroup because there appears to be an indication of a subclinical diagnosis. To provide adequate intervention, future research and clinical practice should distinguish between different risky drinking patterns.