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Nutrigenomics and nutrigenetics in metabolic-(dysfunction) associated fatty liver disease: novel insights and future perspectives

10.15252/emmm.202114753 EMBO Mol Med

Impaired mitochondrial fatty acid oxidation in autism Glutamate-induced mitochondrial dysfunction indirectly and selectively suppresses mitochondrial fatty acid -oxidation.The formation of aspartate from glutamate via the transaminase reaction outcompetes citrate synthase for OAA resulting in a dramatic decrease in citrate and effectively shutting down mitochondrial processing of acetyl-CoA [2].High levels of acetyl-CoA then feedback inhibit mitochondrial -oxidation.Indirectly, the energetic outward transport of aspartate leads to an increased flux through malate dehydrogenase, which causes an increase in the mitochondrial NADH/NAD + ratio, which inhibits -oxidation at the NAD + -linked -hydroxyacyl-CoA dehydrogenase reaction[120].The extra-mitochondrial effects of disrupted mitochondrial fatty acid -oxidation are related to the carnitine-dependency of this system.Carnitine performs two essential metabolic functions.Its primary and most widely recognized function is to shuttle fatty acids (palmitate (16:0) and stearate (18:0)) from the cytosol into the mitochondrial matrix where it can be -oxidized to acetyl-CoA.Its secondary, less recognized function is to shuttle excess acetyl-CoA out of the mitochondrial matrix to the cytosol (for reviews see [121-124])

These findings suggest that L-carnitine is a useful addition to fertility treatments, and combining it with other antioxidants may further enhance reproductive outcomes for men dealing with infertility