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Resistance exercise‐induced increase in muscle 5α‐dihydrotestosterone contributes to the activation of muscle Akt/mTOR/p70S6K‐ and Akt/AS160/GLUT4‐signaling pathways in type 2 diabetic rats
Author(s) -
Horii Naoki,
Hasegawa Natsuki,
Fujie Shumpei,
Uchida Masataka,
Iemitsu Motoyuki
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.201903223rr
Subject(s) - glut4 , protein kinase b , pi3k/akt/mtor pathway , pten , insulin resistance , chemistry , signal transduction , endocrinology , medicine , diabetes mellitus , biochemistry
Effects of increase in muscle 5α‐dihydrotestosterone (DHT) levels caused by resistance exercise on regulation of mammalian target of rapamycin (mTOR)‐ and glucose transporter 4 (GLUT4)‐signaling pathways in type 2 diabetic rats were assessed. Twenty‐week‐old type 2 diabetic rats were randomly divided into the resting control, immediately, 1 hour, or 3 hours after resistance exercise, with or without the pretreatment of 5α‐reductase inhibitor. Immediately or 1 hour after exercise, levels of 5α‐reductase and DHT as well as phosphorylation levels of AMP‐activated protein kinase (AMPK), TBC1 domain family member 1 (TBC1D1), and protein kinase B (Akt) in muscle were significantly elevated. Phosphorylation of muscle Akt substrate of 160 kDa (AS160) and translocation levels of GLUT4 at 1 and 3 hours after resistance exercise were significantly elevated. Additionally, resistance exercise significantly activated the phosphorylation of muscle mTOR immediately, and at 1 and 3 hours and of p70 ribosomal S6 kinase (p70S6K) at 1 and 3 hours. However, pretreatment with the 5α‐reductase inhibitor significantly attenuated the exercise‐induced activation of Akt/mTOR/p70S6K and Akt/AS160/GLUT4 signaling, but did not affect AMPK/TBC1D1/GLUT4 signaling. These findings suggest that resistance exercise‐induced increase in muscle DHT synthesis may contribute to activation of Akt/mTOR/p70S6K‐ and Akt/AS160/GLUT4 signaling pathways in type 2 diabetic rats.