Hyperglycemia inhibits recovery from disuse-induced skeletal muscle atrophy in rats
Language English Country Czech Republic Media print-electronic
Document type Journal Article
PubMed
24702496
DOI
10.33549/physiolres.932687
PII: 932687
Knihovny.cz E-resources
- MeSH
- Atrophy MeSH
- Diabetes Mellitus, Experimental metabolism pathology MeSH
- Hyperglycemia pathology MeSH
- Insulin-Like Growth Factor I metabolism MeSH
- Insulin blood MeSH
- Capillaries pathology ultrastructure MeSH
- Muscle Fibers, Skeletal pathology ultrastructure MeSH
- Muscle, Skeletal pathology MeSH
- Blood Glucose metabolism MeSH
- Rats MeSH
- Rats, Wistar MeSH
- Muscular Disorders, Atrophic pathology MeSH
- Body Weight drug effects MeSH
- Vascular Endothelial Growth Factor A metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Insulin-Like Growth Factor I MeSH
- Insulin MeSH
- Blood Glucose MeSH
- Vascular Endothelial Growth Factor A MeSH
The purpose of this study was to evaluate the effects of hyperglycemia on skeletal muscle recovery following disuse-induced 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.
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