A potential limitation is that acetate wasadministered intravenously, whereas in naturalistic drinking,acetate is produced hepatically:
Are the implication of administering acetate a different route great enough to muddy the results? How might it look different?
Alterations in acetate consumption are not unprecedented:Type 1 diabetes with hypoglycemia unawareness have beenshown to be associated with elevated acetate consumption
How does evidence from type 1 diabetes help interpret the alcohol related findings? Does this put those with type 1 diabetes at higher risk?
we observed differences in brain acetatemetabolism depending on alcohol exposure. Contrary to ourexpectations of dramatically elevated acetate consumption inearly recovery, we saw the opposite
If alcohol elevates circulating acetate and the brain adapts by increasing acetate uptake, why do AUD participants in early abstinence show significantly reduced oxidation instead of elvated use? Does this have to do with impaired transport, competition, or metabolic issues?