Fiche publication
Date publication
juillet 2016
Journal
Biochimie
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis
Tous les auteurs :
Feigerlova E, Demarquet L, Guéant JL
Lien Pubmed
Résumé
Homocysteine (HCY) is a degradation product of the methionine pathway. The B vitamins, in particular vitamin B12 and folate, are the primary nutritional determinant of HCY levels and therefore their deficiencies result in hyperhomocysteinaemia (HHCY). Prevalence of hyperhomocysteinemia (HHCY) and related dietary deficiencies in B vitamins and folate increase with age and have been related to osteoporosis and abnormal development of epiphyseal cartilage and bone in rodents. Here we provide a review of experimental and population studies. The negative effects of HHCY and/or B vitamins and folate deficiencies on bone formation and remodeling are documented by cell models, including primary osteoblasts, osteoclast and bone progenitor cells as well as by animal and human studies. However, underlying pathophysiological mechanisms are complex and remain poorly understood. Whether these associations are the direct consequences of impaired one carbon metabolism is not clarified and more studies are still needed to translate these findings to human population. To date, the evidence is limited and somewhat conflicting, however further trials in groups most vulnerable to impaired one carbon metabolism are required.
Mots clés
Animals, Bone Remodeling, Bone and Bones, metabolism, Carbon, metabolism, Folic Acid, metabolism, Homeostasis, Homocysteine, metabolism, Humans, Hyperhomocysteinemia, metabolism, Osteoblasts, metabolism, Osteoclasts, metabolism, Vitamin B 12, metabolism, Vitamin B Deficiency, metabolism
Référence
Biochimie. 2016 Jul;126:115-23
