Attenuation of exercise-induced heat shock protein 72 expression blunts improvements in whole-body insulin resistance in rats with type 2 diabetes.
Heat shock proteins (HSPs) play an important role in insulin resistance and improve the cellular stress response via HSP induction by exercise to treat type 2 diabetes. In this study, the effects of exercise-induced HSP72 expression levels on whole-body insulin resistance in type 2 diabetic rats were investigated. Male 25-week-old Otsuka Long-Evans Tokushima Fatty rats were divided into three groups: sedentary (Sed), trained in a thermal-neutral environment (NTr: 25 °C), and trained in a cold environment (CTr: 4 °C). Exercise training was conducted 5 days/week for 10 weeks. Rectal temperature was measured following each bout of exercise. An intraperitoneal glucose tolerance test (IPGTT) was performed after the training sessions. The serum, gastrocnemius muscle, and liver were sampled 48 h after the final exercise session. HSP72 and heat shock cognate protein 73 expression levels were analyzed by Western blot, and serum total cholesterol, triglyceride (TG), and free fatty acid (FFA) levels were measured. NTr animals exhibited significantly higher body temperatures following exercise, whereas, CTr animals did not. Exercise training increased HSP72 levels in the gastrocnemius muscle and liver, whereas, HSP72 expression was significantly lower in the CTr group than that in the NTr group (p < 0.05). Glucose tolerance improved equally in both trained animals; however, insulin levels during the IPGTT were higher in CTr animals than those in NTr animals (p < 0.05). In addition, the TG and FFA levels decreased significantly only in NTr animals compared with those in Sed animals. These results suggest that attenuation of exercise-induced HSP72 expression partially blunts improvement in whole-body insulin resistance and lipid metabolism in type 2 diabetic rats.
Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan.|Research Fellow of the Japan Society for the Promotion of Science, Tokyo, 102-0083, Japan.
Takamasa
T
Tsuzuki
Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan.|Department of General Medicine, Mito Medical Center, Tsukuba University Hospital, Ibaraki, 310-0015, Japan.
Hiroyuki
H
Kobayashi
Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan.
Toshinori
T
Yoshihara
Faculty of Medicine, Juntendo University, Tokyo, 113-8421, Japan.
Ryo
R
Kakigi
Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan.|Faculty of Liveral Arts, The Open University of Japan, Chiba, 261-8586, Japan.
Noriko
N
Ichinoseki-Sekine
Graduate School of Health and Sports Science, Juntendo University, Chiba, 270-1695, Japan. hnaitou@juntendo.ac.jp.
Hisashi
H
Naito
D000818:Animals; D019540:Area Under Curve; D001831:Body Temperature; D002784:Cholesterol / Q000097:blood; D003924:Diabetes Mellitus, Type 2 / Q000378:metabolism / Q000473:pathology*; D004195:Disease Models, Animal; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005951:Glucose Tolerance Test; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism; D018482:Muscle, Skeletal / Q000378:metabolism; D010805:Physical Conditioning, Animal; D012372:ROC Curve; D051381:Rats; D020318:Rats, Long-Evans; D013696:Temperature; D014280:Triglycerides / Q000097:blood
D005230:Fatty Acids, Nonesterified; D050884:HSP72 Heat-Shock Proteins; D007328:Insulin; D014280:Triglycerides; D002784:Cholesterol
Body temperature; Exercise training; Heat shock protein; Insulin resistance; Type 2 diabetes