Voluntary Exercise Can Ameliorate Insulin Resistance by Reducing iNOS-Mediated S-Nitrosylation of Akt in the Liver in Obese Rats
View/ Open
Author
Tsuzuki, Takamasa
Shinozaki, Shohei
Nakamoto, Hideko
Goto, Sataro
Shimokado, Kentaro
Kobayashi, Hiroyuki
Naito, Hisashi
Published Version
https://doi.org/10.1371/journal.pone.0132029Metadata
Show full item recordCitation
Tsuzuki, Takamasa, Shohei Shinozaki, Hideko Nakamoto, Masao Kaneki, Sataro Goto, Kentaro Shimokado, Hiroyuki Kobayashi, and Hisashi Naito. 2015. “Voluntary Exercise Can Ameliorate Insulin Resistance by Reducing iNOS-Mediated S-Nitrosylation of Akt in the Liver in Obese Rats.” PLoS ONE 10 (7): e0132029. doi:10.1371/journal.pone.0132029. http://dx.doi.org/10.1371/journal.pone.0132029.Abstract
Voluntary exercise can ameliorate insulin resistance. The underlying mechanism, however, remains to be elucidated. We previously demonstrated that inducible nitric oxide synthase (iNOS) in the liver plays an important role in hepatic insulin resistance in the setting of obesity. In this study, we tried to verify our hypothesis that voluntary exercise improves insulin resistance by reducing the expression of iNOS and subsequent S-nitrosylation of key molecules of glucose metabolism in the liver. Twenty-one Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus, and 18 non-diabetic control Long-Evans Tokushima Otsuka (LETO) rats were randomly assigned to a sedentary group or exercise group subjected to voluntary wheel running for 20 weeks. The voluntary exercise significantly reduced the fasting blood glucose and HOMA-IR in the OLETF rats. In addition, the exercise decreased the amount of iNOS mRNA in the liver in the OLETF rats. Moreover, exercise reduced the levels of S-nitrosylated Akt in the liver, which were increased in the OLETF rats, to those observed in the LETO rats. These findings support our hypothesis that voluntary exercise improves insulin resistance, at least partly, by suppressing the iNOS expression and subsequent S-nitrosylation of Akt, a key molecule of the signal transduction pathways in glucose metabolism in the liver.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4501761/pdf/Terms of Use
This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAACitable link to this page
http://nrs.harvard.edu/urn-3:HUL.InstRepos:17820954
Collections
- HMS Scholarly Articles [17918]
Contact administrator regarding this item (to report mistakes or request changes)