Asprosin promotes β-cell apoptosis by inhibiting the autophagy of β-cell via AMPK-mTOR pathway

Asprosin is a newly discovered adipokine. A recent study showed that asprosin promoted the beta-cell apoptosis of MIN6 cells. This study aims to determine whether asprosin induces the apoptosis in beta-cell via regulating autophagy. Mouse insulinoma MIN6 cells were divided into the following four groups: control, vehicle, high glucose, and asprosin groups. MIN6 cells in the asprosin group were transfected with recombinant asprosin-T2A-GFP vector. MIN6 cells in the vehicle group were transfected with vector only. Then the apoptosis of MIN6 cells was detected using flow cytometry. Real-time polymerase chain reaction and western blot were used to determine the expression of caspase 3, LC3-I, LC3-II, beclin 1, P62, AMP activated protein kinase (AMPK), and mammalian target of rapamycin (mTOR). AMPK pathway was enhanced using AMPK agonist AICAR. High glucose and asprosin induced the apoptosis of MIN6 cells and elevated expression of caspase 3. In addition, high glucose and asprosin resulted in reduced expression of LC3-II/LC3-I, beclin 1, and increased expression of P62. p-AMPK expression was decreased and p-mTOR expression was increased after high glucose and asprosin treatment. AMPK agonist AICAR was used to activate the AMPK pathway. Treatment with AICAR significantly partly restored decreased autophagy and increased apoptosis of beta-cell, which was induced by asprosin. Asprosin promotes the apoptosis of beta-cell by inhibiting the autophagy of beta-cell via AMPK-mTOR pathway.

Automated summary

The study demonstrated that asprosin induces apoptosis in beta-cells by inhibiting autophagy. High glucose and asprosin both lead to increased apoptosis and altered expression of certain proteins in MIN6 cells, affecting the AMPK-mTOR signaling pathway. Activation of the AMPK pathway by AICAR partially reverses the effects of asprosin on autophagy and apoptosis in beta-cells.