**4. Concluding Remarks**

VitC homeostasis is tightly regulated by a variety of more or less specific transport mechanisms, some of which may remain to be established. Several *in vitro* and *in vivo* studies have reported dose- and concentration-dependent rates of transport, both during ASC depletion and following supplementation, and these changes in transport activity apparently occur without change in affinity for the substrate. However, conflicting evidence has also been put forward in which the resulting changes in tissue compartment concentrations cannot be explained by alterations in the abundance of known vitC transporters. Moreover, as genetic variation has been shown to significantly influence vitC homeostasis *per se*, such information needs to be taken into consideration in future studies. Thus, continued efforts are required to establish the mechanisms by which the body efficiently adapts to declining vitC intakes.
