Heat stress prevents the decrease in succinate dehydrogenase activity in the extensor digitorum longus of streptozotocin-induced diabetic rats

Title:

Heat stress prevents the decrease in succinate dehydrogenase activity in the extensor digitorum longus of streptozotocin-induced diabetic rats

Creator:

Nonaka, K, Une, S, Akiyama, J, Yamaji, R, and Komatsu, M

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:639377d6-8632-4a90-8269-c72800a2605b
uuid:639377d6-8632-4a90-8269-c72800a2605b
issn:0862-8408

Subject:

fyziologie člověka, human physiology, Diabetes mellitus, Heat stress, Succinate dehydrogenase, Heat shock protein 60, Superoxide dismutase 2, 14, and 612

Type:

model:article and TEXT

Format:

print, bez média, and svazek

Description:

This study aimed to investigate whether heat stress (HS) prevents a decrease in succinate dehydrogenase (SDH) activity and heat shock protein 60 (HSP60) and superoxide dismutase 2 (SOD2) contents in the extensor digitorum longus of streptozotocin (STZ)-induced diabetic rats. Twelve-week-old male Wistar rats were assigned to one of the four groups (n=6/group): control (Con), HS, diabetes mellitus (DM), and diabetes mellitus and heat stress (DM+HS). Diabetes was induced by the administration of STZ (50 mg/kg). HS was initiated 7 days after STZ treatment and performed at 42 °C for 30 min 5 times a week for 3 weeks. SDH activity was decreased in the DM and DM+HS groups. However, SDH activity was greater in the DM+HS group than in the DM group. Although HSP60 content was lower in the DM group than in the Con group, it was maintained in the DM+HS groups and was higher than that in the DM group. SOD2 content was decreased only in the DM group. These findings suggest that HS prevents the decrease in SDH activity in the skeletal muscle induced by DM. According to this mechanism, the maintenance of SOD2 and HSP60 by HS may suppress the increase in oxidative stress., K. Nonaka, S. Une, M. Komatsu, R. Yamaji, J. Akiyama., and Seznam literatury

Language:

English

Rights:

http://creativecommons.org/publicdomain/mark/1.0/
policy:public

Source:

Physiological research | 2018 Volume:67 | Number:1

Harvested from:

CDK

Metadata only:

false