Hyperinsulinemia contributes to impaired-glucose-tolerance-induced renal injury via mir-7977/SIRT3 signaling.
Zhongai GaoZiyan WangHong ZhuXinxin YuanMengdi SunJingyu WangMinxia ZuoXiao CuiYing HanYi ZhangShaohua YangYongzhang QinJie XuJuhong YangBao Cheng ChangPublished in: Therapeutic advances in chronic disease (2020)
In conclusion, IGT-RI mainly manifests as tubular injury, especially reabsorption dysfunction. Compensatory hyperinsulinemia may be involved. A high level of insulin can activate mir-7977/SIRT3 signaling, resulting in tubular injury by inducing oxidative stress as well as reabsorption dysfunction by inhibiting the expression of cubilin, ultimately contributing to IGT-RI.