You can get there from here: acetone, anionic ketones and even-carbon fatty acids can provide substrates for gluconeogenesis.
Level 5 - mechanism / opinion, no new human data
Narrative review of biochemical pathways with no new experimental data or systematic synthesis.
What was done
This paper reviewed established biochemical literature to delineate the enzymatic reactions and metabolic pathways through which acetone—originating from the non-enzymatic breakdown of acetoacetate during ketosis or from isopropanol oxidation—is converted into gluconeogenic precursors in humans.
What was found
The abstract provides no numerical data, quantitative flux rates, or sample statistics. It qualitatively reports that acetone is not a metabolic dead end, but rather can be converted into D-lactate and pyruvate, which subsequently feed into gluconeogenesis to produce glucose.
Why it matters
This review clarifies a common misconception in textbook biochemistry by detailing the pathways showing that ketone-derived acetone and even-carbon fatty acid metabolites can ultimately contribute to glucose synthesis.
Limits
The abstract reports no primary experimental data, quantitative metabolic flux measurements, or systematic methodology. Quantitative clinical significance and the actual physiological contribution of this pathway in vivo cannot be evaluated from this record.
Cited by
- contradicts Acetone cannot be mobilized by the human body as fuel and is exhaled as a waste product through the lungs.