PPARγ agonists exert additional positive effects on neuronal energy balance by stimulating GLUT3 expression (Garcia-Bueno et al., 2006; Wang et al., 2012), which is decreased in AD (Simpson et al., 1994), by stimulating GLUT4-mediated glucose uptake and by promoting neuronal lactate oxidation (Izawa et al., 2009) and pyruvate flux (Rossi et al., 2020) via enhancing insulin-stimulated Akt activation (Karwi et al., 2020) and inhibiting PDH kinase activity (Way et al., 2001). This evidence concerns the gene INS and Alzheimer disease.