Effect of Articular Immobilization - Induced Hindlimb Skeletal Muscle Atrophy on Autophosphorylation of Tyrosine Kinase of the Insulin Receptor in Rats.
- Author:
Dae Mang KIM
;
Jong Chul AHN
;
Jong Youn KIM
;
Suck Kang LEE
- Publication Type:Original Article
- Keywords:
Hindlimb skeletal muscle;
Atrophy;
Immobilization;
Autophosphorylation of tyrosine kinase of insulin receptor
- MeSH:
Animals;
Ankle Joint;
Atrophy*;
Body Weight;
Glycogen;
Hindlimb*;
Immobilization*;
Insulin Resistance;
Insulin*;
Knee;
Muscle, Skeletal*;
Protein-Tyrosine Kinases*;
Rats*;
Receptor, Insulin*;
Tyrosine*
- From:The Journal of the Korean Orthopaedic Association
1997;32(1):177-183
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
The purpose of this study was to investigate the effects of articular immobilization-induced hindlimb skeletal muscle atrophy on the autophosphorylation of the insulin receptor tyrosine kinase in rats. Rats were divided control, and knee and ankle joint immobilized groups. The experiments were performed on the 3rd, 7th, and 21st day after the immobilization. immobilization was induced by k-wire fixation in knee and ankle joint. The ratio of soleus muscle weight to body weight was decreased in proportion to the duration of the immobilization. The glycogen content of the soleus muscle was decreased significantly (p<0.01) at the 7th day, but this value was recovered to 65% of control at the 21st day after the immobilization. The insulin bindings at various concentrations of insulin to wheat-germ agglutinin purified insulin receptor from red gastrocnemius muscle at the 7th day after immobilization were not changed compared to control. The autophosphorylation of the insulin receptor tyrosine kinase with 10-8 and 10-7 M insulin concentration at the 7th day after immobilization was decreased compared to control. In conclusion, above results showed that insulin resistance of immobilized rat hindlimb skeletal muscle was arised from defect of autophosphorylation of the insulin receptor tyrosine kinase in part.
