I know that oxaloacetate cannot cross the mitochondrial membrane, but can instead be converted to aspartate, shuttled out, and then re-converted back to oxaloacetate. What does this have to do with gluconeogenesis?
The traditional route is to convert pyruvate to OAA to malate in the mitochondria, shuttle the malate out, and then convert malate back to OAA in the cytosol. If lactate is the precursor, then the conversion of lactate to pyruvate in the cytosol can generate an NADH, making the conversion to malate in the mitochondria unnecessary. Thus, OAA is converted directly to PEP in the mitochondria by mitochondrial PEPCK and shuttled out to the cytosol to begin gluconeogenesis.
If we have these two pathways, what is the point of using aspartate?