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David Plaut: Off the Cuff

Humans, Guinea Pigs and Bats

Published August 20, 2014 2:58 PM by David Plaut

Why can humans (and guinea pigs and dry-nosed primates and bats) not make vitamin C and are thus open to scurvy without replacement?

Many years ago, I worked on a study of guinea pigs that had been fed a diet without vitamin C and thus developed scurvy.  I knew that people, like the guinea pigs, could develop scurvy without adding the vitamin to our diet.  This has been known for more than a century and in the last few years we have found out why it happens to these few animals.

The inability of humans to synthesize L-ascorbic acid is known to be due to a lack of an enzyme that is required for the biosynthesis of this vitamin. The enzyme is known as L-gulono-gamma-lactone oxidase (GULO). Isolation of a cDNA for the rat enzyme resulted in a study of the basic defect underlying this deficiency at the gene level and led to isolation of a human genomic clone related to L-gulono-gamma-lactone oxidase as well as three overlapping clones covering the entire coding region of the rat L-gulono-gamma-lactone oxidase cDNA. Sequence analysis study indicated that the human L-gulono-gamma-lactone oxidase gene has accumulated a large number of mutations since it stopped being active and that it now exists as a pseudogene in the human genome.

This genetic defect has not been selected against in natural selection as we are able to consume more than enough vitamin C from our diet. It is also suggested that organisms without a functional GULO gene have a method of "recycling" the vitamin C that they obtain from their diets using red blood cells.

References

  1. Cell. 2008 Mar 21;132(6):1039-48
  2. Hum Gene Ther. 2008 Dec;19(12):1349-58
  3. Am J Clin Nutr. 1991 Dec;54(6 Suppl):1203S-1208S.
posted by David Plaut

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