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Int. J. Mol. Sci. 2015, 16(9), 22856-22869; doi:10.3390/ijms160922856

The Role of PTP1B O-GlcNAcylation in Hepatic Insulin Resistance

1
Department of Endocrinology, Affiliated Hospital of Nantong University, Nantong 226001, China
2
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong 226001, China
3
Co-Innovation Center of Neuroregeneration, Nantong University, Nantong 226001, China
These authors contributed equally to this work.
*
Authors to whom correspondence should be addressed.
Academic Editor: Patricia Berninsone
Received: 11 May 2015 / Revised: 1 September 2015 / Accepted: 16 September 2015 / Published: 22 September 2015
(This article belongs to the Special Issue Glycosylation and Glycoproteins)
View Full-Text   |   Download PDF [4330 KB, uploaded 22 September 2015]   |  

Abstract

Protein tyrosine phosphatase 1B (PTP1B), which can directly dephosphorylate both the insulin receptor and insulin receptor substrate 1 (IRS-1), thereby terminating insulin signaling, reportedly plays an important role in insulin resistance. Accumulating evidence has demonstrated that O-GlcNAc modification regulates functions of several important components of insulin signal pathway. In this study, we identified that PTP1B is modified by O-GlcNAcylation at three O-GlcNAc sites (Ser104, Ser201, and Ser386). Palmitate acid (PA) impaired the insulin signaling, indicated by decreased phosphorylation of both serine/threonine-protein kinase B (Akt) and glycogen synthase kinase 3 beta (GSK3β) following insulin administration, and upregulated PTP1B O-GlcNAcylation in HepG2 cells. Compared with the wild-type, intervention PTP1B O-GlcNAcylation by site-directed gene mutation inhibited PTP1B phosphatase activity, resulted in a higher level of phosphorylated Akt and GSK3β, recovered insulin sensitivity, and improved lipid deposition in HepG2 cells. Taken together, our research showed that O-GlcNAcylation of PTP1B can influence insulin signal transduction by modulating its own phosphatase activity, which participates in the process of hepatic insulin resistance. View Full-Text
Keywords: insulin resistance; PTP1B; O-GlcNAc insulin resistance; PTP1B; O-GlcNAc
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Zhao, Y.; Tang, Z.; Shen, A.; Tao, T.; Wan, C.; Zhu, X.; Huang, J.; Zhang, W.; Xia, N.; Wang, S.; Cui, S.; Zhang, D. The Role of PTP1B O-GlcNAcylation in Hepatic Insulin Resistance. Int. J. Mol. Sci. 2015, 16, 22856-22869.

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