Studies
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Following on in silico and in vitro work, the effect of MCAD deficiency on CoA metabolism was investigated. Using a recently published HILIC-MS/MS method, free and acylated CoA species could be measured simultaneously in HepG2 MCAD-KO cells. The levels of CoA biosynthesis intermediates and total CoA was also characterised by HPLC in liver samples from MCAD-KO mice exposed to energetic stress (fasting adn cold). qPCR was applied to investigate changes in the CoA metabolism that might constitute ...
Submitter: Christoff Odendaal
Investigation: Mitochondrial fatty acid oxidation in human liver
Assays: Computational model (in silico), HepG2 cells (in vitro), Mice (in vivo)
Submitter: Christoff Odendaal
Investigation: Mitochondrial fatty acid oxidation in human liver
Assays: Kinetics Minireviews, Models
Submitter: Christoff Odendaal
Investigation: Mitochondrial fatty acid oxidation in human liver
Assays: ACAD activity partitioning, HepG2 oxygen consumption, Whole-body ketogenic flux
Submitter: Christoff Odendaal
Investigation: Mitochondrial fatty acid oxidation in human liver
Assays: Comparing acyl-CoA dehydrogenase deficiencies, MCADD patient personalised modelling, MCADD rescue titration, Metabolic control analysis, Predicting urinary acylcarnitines under metabolic decompensation.
