En un estudio en pacientes con diabetes tipo II, la L-carnitina mejor la respuesta de azcar en sangre a comidas ricas en carbohidratos
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])
Key signaling nodes include JAK/STAT (particularly STAT3), NF-B, and FOXO transcription factors that upregulate muscle ubiquitin ligases (MuRF1/MAFbx), while myostatin/activin ASMAD2/3 signaling via ActRIIB suppresses anabolism
Parker BA, Sturm K, MacIntosh CG, Feinle C, Horowitz M, Chapman IM: Relation between food intake and visual analogue scale ratings of appetite and other sensations in healthy older and young subjects
