Hyperglycemia inhibits recovery from disuse-induced skeletal muscle atrophy in rats
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
24702496
DOI
10.33549/physiolres.932687
PII: 932687
Knihovny.cz E-zdroje
- MeSH
- atrofie MeSH
- experimentální diabetes mellitus metabolismus patologie MeSH
- hyperglykemie patologie MeSH
- insulinu podobný růstový faktor I metabolismus MeSH
- inzulin krev MeSH
- kapiláry patologie ultrastruktura MeSH
- kosterní svalová vlákna patologie ultrastruktura MeSH
- kosterní svaly patologie MeSH
- krevní glukóza metabolismus MeSH
- krysa rodu Rattus MeSH
- potkani Wistar MeSH
- svalové atrofie patologie MeSH
- tělesná hmotnost účinky léků MeSH
- vaskulární endoteliální růstový faktor A metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- insulinu podobný růstový faktor I MeSH
- inzulin MeSH
- krevní glukóza MeSH
- vaskulární endoteliální růstový faktor 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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