therefore, LCACs act as the fatty acid transport moieties for oxidative catabolism Mutations in key enzymes increase mitochondrial and cytosolic pools of long-chain acyl-coenzyme A, promoting an accumulation of LCACs that is diagnostic of fatty acid oxidation disorders LCACs can modulate inflammation, insulin sensitivity, myocyte stress, protein kinase C signalling and ion balance, which suggests that they contribute to both physiological and pathophysiological processes beyond fuel trafficking A model is proposed to explain how LCACs affect disparate cell systems on the basis of their zwitterion biochemical structure and published evidence that they interact with plasma membranes In this model, accumulation of LCACs is predicted to alter the activities of key receptors, transporters, channels and enzymes that associate with (or involve) plasma, mitochondrial or other membranes Abstract Perturbations in metabolic pathways can cause substantial increases in plasma and tissue concentrations of long-chain acylcarnitines (LCACs)
FIGURE 1 Currently, N-acetylcysteine (NAC) is the only U.S
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Lack of NLRP3-inflammasome leads to gut-liver axis derangement, gut dysbiosis and a worsened phenotype in a mouse model of NAFLD
