Genetic animal models to decipher the pathogenic effects of vitamin B12 and folate deficiency.
Fiche publication
Date publication
juillet 2016
Journal
Biochimie
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis, Dr DREUMONT Natacha
Tous les auteurs :
Peng L, Dreumont N, Coelho D, Guéant JL, Arnold C
Lien Pubmed
Résumé
Vitamin B12 and folate are essential micronutrients that provide methyl groups for cellular methylations through the so-called one-carbon metabolism. Deficits in the absorption and transport or defects of the enzymes can lead to human pathogenesis comprising hematologic, neural, gastrointestinal, hepatic, renal, cardiovascular and developmental manifestations. One-carbon metabolism is a complex, multistep and multi-organ metabolism, and the understanding of the mechanisms at work have benefited from human inborn errors and population studies, as well as from nutritional animal models. Since 15 years, a wide variety of genetically engineered mice has been developed and has proved to be useful to decipher the underlying mechanisms. These genetically engineered mice target all the genes that are important for the intestinal absorption, cellular transport and metabolism of vitamin B12 and folate, which are detailed in this article. In conclusion, these mouse models represent valuable experimental paradigms for human pathogenesis. Since no animal model recapitulates the full spectrum of a human disease, researchers have to choose the one that is the most relevant for their specific needs, and this review may help in this respect.
Mots clés
Animals, Disease Models, Animal, Folic Acid Deficiency, genetics, Humans, Mice, Mice, Transgenic, Vitamin B 12 Deficiency, genetics
Référence
Biochimie. 2016 Jul;126:43-51