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Exercise training improves basal blood glucose metabolism with no changes of cytosolic inhibitor κB kinase or c‐Jun N‐terminal kinase activation in skeletal muscle of Otsuka Long–Evans Tokushima fatty rats
Author(s) -
Lee Hojun,
Chang Hyukki,
Park JaeYoung,
Kim SiYoung,
Choi KyungMook,
Song Wook
Publication year - 2011
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2011.057737
Subject(s) - medicine , endocrinology , skeletal muscle , kinase , chemistry , type 2 diabetes , oxidative stress , carbohydrate metabolism , glucose uptake , citrate synthase , diabetes mellitus , insulin , enzyme , biochemistry
Redox‐sensitive stress kinases and heat shock protein 72 (Hsp72) have been considered to be associated with the development of type 2 diabetes in skeletal muscle. However, the effect of exercise training on skeletal muscle of type 2 diabetic models is largely unknown. The purpose of this study was to investigate the effect of 12 weeks of exercise training on gastrocnemius of type 2 diabetic rats, by examining the activation of c‐Jun N‐terminal kinase (JNK), the nuclear factor κB (NF‐κB) pathway and Hsp72. Total hydroperoxide and 4‐hydroxynoneal, as oxidative stress markers, were also examined. Otsuka Long–Evans Tokushima fatty (OLEFT) rats were randomly divided into an exercise training group (Ex‐OLETF, n = 8) and a sedentary group (Sed‐OLETF, n = 8), while Long–Evans Tokushima Otsuka (LETO) rats were used as a control group (Con‐LETO, n = 5). The Ex‐OLETF rats were trained on a treadmill five times a week for 12 weeks. The levels of hydroperoxide and 4‐hydroxynoneal in both Ex‐OLETF and Sed‐OLETF were significantly higher compared with Con‐LETO, but there was no difference between Ex‐OLETF and Sed‐OLETF. Levels of inhibitor κB kinase, JNK activation and p65 nuclear translocation followed a similar pattern to that observed in oxidative stress markers. The level of Hsp72 in Ex‐OLETF was increased by exercise training, but it did not reach the level observed in Con‐LETO. The NF‐κB DNA binding activity in Sed‐OLETF was significantly higher compared with Con‐LETO. Although it was not statistically significant, exercise training in Ex‐OLETF showed a trend to reduce the activation of NF‐κB DNA binding activity compared with Sed‐OLETF ( P = 0.104). Our findings indicate that exercise training improves basal glucose metabolism without a change in stress kinases, and that nuclear regulation of NF‐κB activity in diabetic muscle could be regulated independently of the cytosolic pathway. Our study also suggests a possibility that exercise‐induced Hsp72 serves as a protective mechanism in skeletal muscle of OLETF rats.