BECN1 and metabolic syndrome: Zhu et al. [66] have shown that the iminosugar D-lentiginosine, whose structure is closely similar to that of calystegine B2, stimulated autophagy effectively by upregulating Beclin 1, thus causing the conversion of LC3-I to LC3-II through an inhibition of Akt/mTOR signaling by downregulating the expression of Akt and repressing its phosphorylation; these observations could thus correlate with the fact that calystegines have not exerted any upregulation effect on the Akt gene expression, already repressed under the metabolic syndrome condition.