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doi: 10.1111/j.1600-079X.2006.00353.x

A severe carnitine deficiency is thought to contribute to VHE.[5] Although the precise mechanism leading to hypocarnitinemia in patients treated with valproate is not known, a previous clinical study showed a significant decrease in carnitine concentration and changes in the ratio of acylcarnitine to free carnitine for both neurological and psychiatric indications.[6] Recently, we reported that VPA treatment induces hyperammonemia and causes concentration-dependent carnitine deficiency regardless of the use of additional mood stabilizers, while serum levels of NH3 do not correlate with VPA concentrations in psychiatric patients.[7] In the field of pediatric neurology, reports suggests carnitine supplementation tends to normalize elevated NH3 concentration by binding to VPA and relieving the inhibition of urea synthesis with favorable clinical response.[8,9] In contrast, despite the widespread use of VPA in psychiatry, carnitine supplementation for the treatment of hyperammonemia and hypocarnitinemia has not been prospectively studied in a psychiatric setting

Therefore, a combined model of reactor and metabolism, linking the macrokinetics of the reactor with the cellular microkinetics, was developed, and was demonstrated to be useful for the establishment of genetic engineering strategies [108]