Inhibition of C1-Ten PTPase activity reduces insulin resistance through IRS-1 and AMPK pathways
- Authors
- Jeong, Heeyoon; Koh, Ara; Lee, Jiyoun; Park, Dohyun; Lee, Jung Ok; Lee, Mi Nam; Jo, Kyung-Jin; Huynh Nguyen Khanh Tran; Kim, Eui; Min, Byung-Sun; Kim, Hyeon Soo; Berggren, Per-Olof; Ryu, Sung Ho
- Issue Date
- 19-12월-2017
- Publisher
- NATURE PUBLISHING GROUP
- Citation
- SCIENTIFIC REPORTS, v.7
- Indexed
- SCIE
SCOPUS
- Journal Title
- SCIENTIFIC REPORTS
- Volume
- 7
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/81154
- DOI
- 10.1038/s41598-017-18081-8
- ISSN
- 2045-2322
- Abstract
- Insulin resistance causes type 2 diabetes; therefore, increasing insulin sensitivity is a therapeutic approach against type 2 diabetes. Activating AMP-activated protein kinase (AMPK) is an effective approach for treating diabetes, and reduced insulin receptor substrate-1 (IRS-1) protein levels have been suggested as a molecular mechanism causing insulin resistance. Thus, dual targeting of AMPK and IRS-1 might provide an ideal way to treat diabetes. We found that 15,16-dihydrotanshinone I (DHTS), as a C1-Ten protein tyrosine phosphatase inhibitor, increased IRS-1 stability, improved glucose tolerance and reduced muscle atrophy. Identification of DHTS as a C1-Ten inhibitor revealed a new function of C1-Ten in AMPK inhibition, possibly through regulation of IRS-1. These findings suggest that C1-Ten inhibition by DHTS could provide a novel therapeutic strategy for insulin resistance-associated metabolic syndrome through dual targeting of IRS-1 and AMPK.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
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