How humans make up for an 'inborn' vitamin C deficiency

Then, another surprise: The researchers found that the red cells of mice, a species that can produce vitamin C, don’t carry Glut1 on their red blood cells at all. They carry Glut4 instead. They suspected that the differences in human red blood cells might be linked to our inability to synthesize the reduced form of DHA, vitamin C, from glucose. In fact, they confirmed Glut1 expression on human, guinea pig and fruit bat red blood cells, but not on any other mammalian red cells tested, including rabbit, rat, cat, dog and chinchilla. Next, they took a closer look at primates. Primates belonging to the Haplorrhini suborder (including prosimian tarsiers, new world monkeys, old world monkeys, humans and apes) have lost the ability to synthesize vitamin C, whereas primates in the Strepsirrhini suborder (including lemurs) are reportedly able to produce this vitamin, Taylor explained.

Notably, they detected Glut1 on all tested red blood cells of primates within the higher primate group, including long-tailed macaques, rhesus monkeys, baboons and magot monkeys. In marked contrast, Glut1 was not detected on lemur red blood cells. Moreover, they report, although DHA uptake in human and magot red cells was similar, the level of transport in cells from three different lemur species was less than 10% of that detected in higher primates.

“Red blood cell-specific Glut1 expression and DHA transport are specific traits of the few vitamin C-deficient mammalian species, encompassing only higher primates, guinea pigs and fruit bats,” the researchers concluded. “Indeed, the red cells of adult mice do not harbor Glut1 and do not transport DHA. Rather, Glut4 is expressed on their cells. Thus, the concomitant induction of Glut1 and stomatin during red blood cell differentiation constitutes a compensatory mechanism in mammals that are unable to synthesize the essential ascorbic acid metabolite,” otherwise known as vitamin C.

The researchers include Amelie Montel-Hagen, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; Sandrina Kinet, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; Nicolas Manel, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; Cedric Mongellaz, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; Rainer Prohaska, Max F. Perutz Laboratories, Department of Medical Biochemistry, Medical University of Vienna, Vienna, Austria; Jean-Luc Battini, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; Jean Delaunay, Hematologie, Hopital de Bicetre, APHP, INSERM U779, Faculte´ de Medecine Paris-Sud, Le Kremlin-Bicetre, France; Marc Sitbon, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France; and Naomi Taylor, Institut de Genetique Moleculaire de Montpellier, CNRS, Universite´ Montpellier I and II, Montpellier, France.