Hyperglycemia inhibits recovery from disuse-induced skeletal muscle atrophy in rats

Title:

Hyperglycemia inhibits recovery from disuse-induced skeletal muscle atrophy in rats

Creator:

Kataoka, H., Nakano, J., Morimoto, Y., Honda, Y., Sakamoto, J., Origuchi, T., Okita, M., and Yoshimura, T.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:38813c37-8cc9-4574-91df-916c01d758c5
uuid:38813c37-8cc9-4574-91df-916c01d758c5
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, hyperglykémie, hyperglycemia, disuse-induced muscle atrophy, recovery, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

The purpose of this study was to evaluate the effects of hyperglycemia on skeletal muscle recovery following disuseinduced muscle atrophy in rats. Wistar rats were grouped as streptozotocin-induced diabetic rats and non-diabetic rats. Both ankle joints of each rat were immobilized to induce atrophy of the gastrocnemius muscles. After two weeks of immobilization and an additional two weeks of recovery, tail blood and gastrocnemius muscles were isolated. Serial cross sections of muscles were stained for myosin ATPase (pH 4.5) and alkaline phosphatase activity. Serum insulin and muscle insulin-like growth factor-1 (IGF-1) levels were also measured. Serum insulin levels were significantly reduced in the diabetic rats compared to the non-diabetic controls. The diameters of type I, IIa, and IIb myofibers and capillary-to-myofiber ratio in the isolated muscle tissue were decreased after immobilization in both treatments. During the recovery period, these parameters were restored in the non-diabetic rats, but not in the diabetic rats. In addition, muscle IGF-1 levels after recovery increased significantly in the non-diabetic rats, but not in the diabetic rats. We conclude that decreased levels of insulin and IGF-1 and impairment of angiogenesis associated with diabetes might be partly responsible for the inhibition of regrowth in diabetic muscle., H. Kataoka, J. Nakano, Y. Morimoto, Y. Honda, J. Sakamoto, T. Origuchi, M. Okita, T. Yoshimura., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2014 Volume:63 | Number:4

Harvested from:

CDK

Metadata only:

false