TAB3 involves in hepatic insulin resistance through activation of MAPK pathway

General and Comparative Endocrinology
Yun ZhaoShiwei Cui

Abstract

Insulin resistance is often accompanied by chronic inflammatory responses. The mitogen-activated protein kinase (MAPK) pathway is rapidly activated in response to many inflammatory cytokines. But the functional role of MAPKs in palmitate-induced insulin resistance has yet to be clarified. In this study, we found that transforming growth factor β-activated kinase binding protein-3 (TAB3) was up-regulated in insulin resistance. Considering the relationship between transforming growth factor β-activated kinase (TAK1) and MAPK pathway, we assumed TAB3 involved in insulin resistance through activation of MAPK pathway. To certify this hypothesis, we knocked down TAB3 in palmitate treated HepG2 cells and detected subsequent biological responses. Importantly, TAB3 siRNA directly reversed insulin sensitivity by improving insulin signal transduction. Moreover, silencing of TAB3 could facilitate hepatic glucose uptake, reverse gluconeogenesis and improve ectopic fat accumulation. Meanwhile, we found that the positive effect of knocking down TAB3 was more significant when insulin resistance occurred. All these results indicate that TAB3 acts as a negative regulator in insulin resistance through activation of MAPK pathway.

References

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Citations

Jul 5, 2016·International Journal of Molecular Sciences·Shudong WangYang Zheng
Jan 24, 2017·General and Comparative Endocrinology·Pingli LiuXinhua Ye
Dec 29, 2018·Journal of Diabetes Investigation·Lu LiXi Yang
Dec 20, 2018·Physiological Reviews·Meng XuHongliang Li

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