Bothdietary glucose and fructose can activate the translocation of ChREBP from the cytoplasm tothe nucleus, where it forms heterodimers with Max-like protein X (MLX) in the nucleus andthen combines with target genes containing carbohydrate response elements (ChoREs) [ 58, 59].High-fructose feeding systemic or intestinal-specific knockout ChREBP mice cannot induceGLUT5 expression and exhibit malabsorption syndrome (mainly characterized by diarrhea,weight loss, and intestinal distention), impaired metabolism, decreased body temperature andeven near death within 1–2 weeks [ 60, 61]. The gene discussed is MLXIPL; the disease is malabsorption syndrome.