Pycnogenol (?) In The Regulation Of Hepatic Insulin Resistance And Its Molecular Mechanism

Objective:In recent years,there has been a dramatic increase in the number of people with diabetes in the world.The liver is an important glycolipid metabolism organ.Patients with type 2 diabetes are often associated with hepatic steatosis,which is closely related to insulin resistance,the major pathogenesis of which.Pycnogenol is a French bark pine bark extract with strong anti-oxidant and anti-inflammatory properties.It has been clinically proven to improve the symptoms of diabetes and other metabolic diseases.However,the underlying mechanism remains unclear.Therefore,Pycnogenol fatty liver model of insulin resistance cell model to detect its gluconeogenesis and glycolysis and insulin signaling pathway to explore its role in glucose metabolism and possible molecular mechanisms.Methods: AML12 mouse hepatocytes were treated with OA for 24 hours to establish insulin resistance model.After PYC treatment for 24 hours,glucose metabolism was evaluated by PYC and the residual glucose content in supernatant of medium and PAS staining.And glycolysis-related mRNA expression;Western blot detection of PYC on insulin signaling pathway.Results: PCR treatment of insulin resistance model 24 hours later,the supernatant of the supernatant of glucose in the experimental group was significantly reduced(P <0.05),PAS staining showed the experimental group increased glycogen content.The results of RT-PCR showed that the expression of PKLR in PYC treated group increased(P <0.05),while the other indexes were not statistically significant.Western blot results showed that the expression of P-AKT / AKT and P-GSK-3 in PYC50+ OA group was significantly increased(P <0.05).Conclusion: PYC can improve insulin resistance in liver cells of AML-12 mice and may affect the subsequent glucose metabolism by increasing the expression of P-AKT / AKT,but the process may not be related to gluconeogenesis.However,by increasing PKLR PYC also reduces the peripheral glucose content of the cells by increasing the expression of P-GSK3? to increase the glycogen synthesis of hepatocytes.