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Inhibition of C1-Ten PTPase activity reduces insulin resistance through IRS-1 and AMPK pathways
- Jeong, H (author)
- Koh, A (author)
- Lee, J (author)
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- Park, D (author)
- Lee, JO (author)
- Lee, MN (author)
- Jo, KJ (author)
- Tran, HNK (author)
- Kim, E (author)
- Min, BS (author)
- Kim, HS (author)
- Ryu, SH (author)
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- (creator_code:org_t)
- 2017-12-19
- 2017
- English.
- In: Scientific reports. - : Springer Science and Business Media LLC. - 2045-2322. ; 7:1, s. 17777-
- Journal article (peer-reviewed)
Abstract
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- 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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- Jeong, H
- Koh, A
- Lee, J
- Park, D
- Lee, JO
- Lee, MN
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- Jo, KJ
- Tran, HNK
- Kim, E
- Min, BS
- Kim, HS
- Berggren, PO
- Ryu, SH
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