Children with NAFLD and obesity exhibited an exaggerated metabolic response to fructose administration compared to normal-weight children; this effect was due to the fermentation of fructose to hydrogen by the intestinal bacterial flora or an upregulation of the fructose transporter GLUT5 in the intestinal epithelium [48]. The gene discussed is SLC2A5; the disease is obesity due to melanocortin 4 receptor deficiency.