Document Type
Article
Publication Date
6-13-2017
Abstract
Generalized arterial calcification of infancy (GACI) is an autosomal recessive disorder caused by mutations in the ENPP1 gene. It is characterized by mineralization of the arterial blood vessels, often diagnosed prenatally, and associated with death in early childhood. There is no effective treatment for this devastating disorder. We previously characterized the Enpp1asjmutant mouse as a model of GACI, and we have now explored the effect of elevated dietary magnesium (five-fold) in pregnant mothers and continuing for the first 14 weeks of postnatal life. The mothers were kept on either control diet or experimental diet supplemented with magnesium. Upon weaning at 4 weeks of age the pups were placed either on control diet or high magnesium diet. The degree of mineralization was assessed at 14 weeks of age by histopathology and a chemical calcium assay in muzzle skin, kidney and aorta. Mice placed on high magnesium diet showed little, if any, evidence of mineralization when their corresponding mothers were also placed on diet enriched with magnesium during pregnancy and nursing. The reduced ectopic mineralization in these mice was accompanied by increased calcium and magnesium content in the urine, suggesting that magnesium competes calcium-phosphate binding thereby preventing the mineral deposition. These results have implications for dietary management of pregnancies in which the fetus is suspected of having GACI. Moreover, augmenting a diet with high magnesium may be beneficial for other ectopic mineralization diseases, including nephrocalcinosis.
Recommended Citation
Kingman, Joshua; Uitto, Jouni; and Li, Qiaoli, "Elevated dietary magnesium during pregnancy and postnatal life prevents ectopic mineralization in Enpp1asj mice, a model for generalized arterial calcification of infancy." (2017). Department of Dermatology and Cutaneous Biology Faculty Papers. Paper 78.
https://jdc.jefferson.edu/dcbfp/78
Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.
PubMed ID
28402956
Comments
This article has been peer reviewed. It is the author’s final published version in Oncotarget
Volume 8, Issue 24, June 2017, Pages 38152-38160.
The published version is available at DOI: 10.18632/oncotarget.16687. Copyright © Kingman et al.