@article{APS4240,
author = {Feng Liu and Tao Yang and Bin Wang and Min Zhang and Nan Gu and Jie Qiu and Hong-qi Fan and Chun-mei Zhang and Li Fei and Xiao-qing Pan and Mei Guo and Rong-hua Chen and Xi-rong Guo},
title = {Resistin induces insulin resistance, but does not affect glucose output in rat-derived hepatocytes},
journal = {Acta Pharmacologica Sinica},
volume = {29},
number = {1},
year = {2016},
keywords = {},
abstract = {Aim: The aim of the present study was to observe the effects of resistin on insulin sensitivity and glucose output in rat-derived hepatocytes.
Methods: The rat hepatoma cell line H4IIE was cultured and stimulated with resistin; supernant glucose and glycogen content were detected. The insulin receptor substrate (IRS)-1 and IRS-2, protein kinase B/Akt, glycogen synthase kinase-3b (GSK-3b), the suppressor of cytokine signaling 3 (SOCS-3) protein content, as well as the phosphorylation status were assessed by Western blotting. Specific antisense oligodeoxynucleotides directed against SOCS-3 were used to knockdown SOCS-3.
Results: Resistin induced insulin resistance, but did not affect glucose output in rat hepatoma cell line H4IIE. Resistin attenuated multiple effects of insulin, including insulin-stimulated glycogen synthesis and phosphorylation of IRS, protein kinase B/Akt, as well as GSK-3b. Resistin treatment markedly induced the gene and protein expression of SOCS-3, a known inhibitor of insulin signaling. Furthermore, a specific antisense oligodeoxynucleotide directed against SOCS-3 treatment prevented resistin from antagonizing insulin action.
Conclusion: The major function of resistin on liver is to induce insulin resistance. SOCS-3 induction may contribute to the resistin-mediated inhibition of insulin signaling in H4IIE hepatocytes.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/4240}
}