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The effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats
Author(s) -
Tsuzuki Takamasa,
Kobayashi Hiroyuki,
Naito Hisashi,
Katamoto Shizuo
Publication year - 2011
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/fasebj.25.1_supplement.lb593
Subject(s) - ampk , medicine , skeletal muscle , endocrinology , soleus muscle , amp activated protein kinase , western blot , intraperitoneal injection , type 2 diabetes , chemistry , diabetes mellitus , phosphorylation , protein kinase a , biochemistry , gene
In previous study, heat treatment and AMPK activation by exercise improved glucose tolerance in rat. PURPOSE To determine the effects of heat treatment on AMPK activation in skeletal muscle in type 2 diabetic rats. METHODS Otsuka Long‐Evans Tokushima Fatty rat (OLETF: n=16, 305.3±11.4g), an accurate animal model for human type 2 diabetes, and their counter parts (LETO: n=8, 226.7±14.1g) were used. Sixteen OLETF rats were divided into two groups; Control (n=8: CON) and Heat treatment (n=8: HT). HT received a lower‐body heat treatment (41 °C for 20 min) using water bath under anesthesia once a week for twelve weeks. An intraperitoneal glucose tolerance test was performed for each group in week‐11. In week‐12, the soleus muscles were removed 48 h after the last heat treatment. Phospho‐AMPK and total‐AMPK in the muscle was determined by Western blot analysis. RESULTS At 120 min after glucose injection, blood glucose levels of CON and HT were significantly higher than LETO, whereas blood glucose level of HT was lower than CON. AMPK phosphorylation ratio in the soleus muscle of CON was significantly lower than LETO. However, heat treatment significantly increased AMPK phosphorylation ratio in HT compared with CON, and there was no significant difference between LETO and HT. CONCLUSION Our results indicate that weekly heat treatment for twelve weeks could increase AMPK activation in skeletal muscle in type 2 diabetic rats.