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In vitro experiments showed that didymin inhibited human recombinant aldose reductase (HRAR), rat lens aldose reductase (RLAR), α-glucosidase, and AGE formation. It also activated the insulin-signaling pathway and resulted in improved insulin sensitivity. Together, these physiological effects led to a potent antidiabetic effect. Regarding the molecular mechanisms related to these effects, didymin reduced the expression of protein tyrosine phosphatase (PTP1B) and increased the phosphorylation of IRS-1, PI3K, glycogen synthase kinase 3β (GSK3β), and Akt, besides reducing two key enzymes, leading to diminished hepatic glucose production in insulin-resistant HepG2 cells. Molecular docking studies indicated that didymin possessed high affinity and tight binding capacity for the active sites of HRAR, RLAR, PTP1B, and α-glucosidase. Additionally, didymin showed important vascular effects through the activation of molecular pathways that result in glycemic control, highlighting the great therapeutic potential for diabetes and diabetes-associated complications. Thus, further clinical trials are warranted to investigate the use of didymin as a potential lead candidate to protect against metabolic disorders targeting various organs.
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