Consequences of Loss
It looks likely that some level of adaptation occurred after the loss of the GULO gene by primates. Erythrocyte Glut1 and associated dehydroascorbic acid uptake modulated by stomatin switch are unique traits of humans and the few other mammals that have lost the ability to synthesize ascorbic acid from glucose. As GLUT transporters and stomatin are ubiquitously distributed in different human cell types and tissues, similar interactions can be hypothesized to occur in human cells other than erythrocytes.
Pauling observed that after the loss of endogenous ascorbate production, apo(a) and Lp(a) were greatly favored by evolution, acting as ascorbate surrogate, since the frequency of occurrence of elevated Lp(a) plasma levels in species that had lost the ability to synthesize ascorbate is great. Also, only primates share regulation of CAMP gene expression by vitamin D which occurred after the loss of GULO gene.
Johnson et al. have hypothesized that the mutation of L-gulono lactone oxidase may have been of benefit to early primates by increasing uric acid levels and enhancing fructose effects on weight gain and fat accumulation. With a shortage of food supplies this gave mutants survival advantage.
Grano and De Tullio proposed that organisms that have lost vitamin C biosynthesis have an advantage in that they can finely regulate HIF1α activation on the basis of the dietary intake of vitamin C: with sufficient supply of vitamin C, the HIF transcription factor is less active than in conditions of vitamin C deficiency; the lack of vitamin C biosynthesis may allow our bodies to know more about our nutritional status and consequently set the proper baseline of HIF1α expression acting like a sensitive titration system.
Calabrese proposed that "the loss of an ability to synthesize ascorbic acid in humans...may have been a critical preadaptation which markedly enhanced the survival of early man with a G6PD deficiency living in a malarial infested environment". He based his observation on evidence which indicates that G6PD deficient individuals display enhanced sensitivity to ascorbic acid induced hemolysis.
Read more about this topic: L-gulonolactone Oxidase
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