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Future translational efforts should pursue several directions: first, conducting deep-phenotyping trials in biopsy-confirmed MASH patients, using positron emission tomography to quantify hepatic glucose uptake and correlating these findings with intrahepatic insulin signaling (e.g., p-AKT)

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This finding could also explain the association between ASD and children with propionic acidemia, an inborn error of metabolism [69]

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Reduced basal NO-mediated dilation and decreased endothelial NO-synthase expression in coronary vessels of spontaneously hypertensive rats