Fig. 4From: Personalised modelling of clinical heterogeneity between medium-chain acyl-CoA dehydrogenase patientsComparison of different ACAD deficiencies in silico. The behaviour of one control and three different ACADD computational models of mFAO are shown. The residual activity reflects typical symptomatic patients: 0% for MCADD and SCADD, and 10% for VLCADD. All other ACADs have 100% of control activity. A Model mitochondrial acyl-CoA profile at 150 µM cytosolic palmitoyl-CoA. B NADH production flux at 150 µM cytosolic palmitoyl-CoA. C Steady-state mitochondrial CoASH. Inset gives the same data with a smaller y-axisBack to article page