| Literature DB >> 30982613 |
Silvia Radenkovic1, Matthew J Bird2, Tim L Emmerzaal3, Sunnie Y Wong4, Catarina Felgueira5, Kyle M Stiers6, Leila Sabbagh4, Nastassja Himmelreich7, Gernot Poschet8, Petra Windmolders5, Jan Verheijen9, Peter Witters10, Ruqaiah Altassan11, Tomas Honzik12, Tuba F Eminoglu13, Phillip M James14, Andrew C Edmondson15, Jozef Hertecant16, Tamas Kozicz17, Christian Thiel7, Pieter Vermeersch18, David Cassiman19, Lesa Beamer6, Eva Morava20, Bart Ghesquière21.
Abstract
Phosphoglucomutase 1 (PGM1) encodes the metabolic enzyme that interconverts glucose-6-P and glucose-1-P. Mutations in PGM1 cause impairment in glycogen metabolism and glycosylation, the latter manifesting as a congenital disorder of glycosylation (CDG). This unique metabolic defect leads to abnormal N-glycan synthesis in the endoplasmic reticulum (ER) and the Golgi apparatus (GA). On the basis of the decreased galactosylation in glycan chains, galactose was administered to individuals with PGM1-CDG and was shown to markedly reverse most disease-related laboratory abnormalities. The disease and treatment mechanisms, however, have remained largely elusive. Here, we confirm the clinical benefit of galactose supplementation in PGM1-CDG-affected individuals and obtain significant insights into the functional and biochemical regulation of glycosylation. We report here that, by using tracer-based metabolomics, we found that galactose treatment of PGM1-CDG fibroblasts metabolically re-wires their sugar metabolism, and as such replenishes the depleted levels of galactose-1-P, as well as the levels of UDP-glucose and UDP-galactose, the nucleotide sugars that are required for ER- and GA-linked glycosylation, respectively. To this end, we further show that the galactose in UDP-galactose is incorporated into mature, de novo glycans. Our results also allude to the potential of monosaccharide therapy for several other CDG.Entities:
Keywords: CDG; PGM1-CDG; central carbon metabolism; galactose; glycosylation; mitochondria; nucleotide sugars; tracer metabolomics
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Year: 2019 PMID: 30982613 PMCID: PMC6506806 DOI: 10.1016/j.ajhg.2019.03.003
Source DB: PubMed Journal: Am J Hum Genet ISSN: 0002-9297 Impact factor: 11.025