| Full text | |
| Author(s): |
Pinheiro-Dardis, Clara Maria
[1]
;
Gutierres, Vania Ortega
[1]
;
Assis, Renata Pires
[1]
;
Peviani, Sabrina Messa
[2]
;
Delfino, Gabriel Borges
[2]
;
Quagliotti Durigan, Joao Luiz
[3]
;
Salvini, Tania de Fatima
[2]
;
Baviera, Amanda Martins
[1]
;
Brunetti, Iguatemy Lourenco
[1]
Total Authors: 9
|
| Affiliation: | [1] Sao Paulo State Univ UNESP, Sch Pharmaceut Sci, Dept Clin Anal, Araraquara, SP - Brazil
[2] Fed Univ Sao Carlos UFSCar, Dept Phys Therapy, Sao Carlos, SP - Brazil
[3] Univ Brasilia, Phys Therapy Div, Brasilia, DF - Brazil
Total Affiliations: 3
|
| Document type: | Journal article |
| Source: | THERAPEUTICS AND CLINICAL RISK MANAGEMENT; v. 14, p. 275-286, 2018. |
| Web of Science Citations: | 1 |
| Abstract | |
Background: The aim of this study was to evaluate the changes in biomarkers of skeletal muscle proteolysis (atrogin-1, muscle RING finger-1 protein {[}MuRF-1]) and inflammation (nuclear factor kappa-B) in skeletal muscles of rats under two catabolic conditions, diabetes mellitus (DM) and acute joint inflammation, and the effects of insulin therapy. Materials and methods: Male Wistar rats were divided into groups without diabetes - normal (N), saline (NS), or iota-carrageenan (NCa) injection into the tibiotarsal joint - and groups with diabetes - diabetes (D), plus insulin (DI), saline (DS), or iota-carrageenan (DCa) injection into the tibiotarsal joint, or iota-carrageenan injection and treatment with insulin (DCaI). Three days after iota-carrageenan injection (17 days after diabetes induction), tibialis anterior (TA) and soleus (SO) skeletal muscles were used for analysis. Results: DM alone caused a significant decrease in the mass of TA and SO muscles, even with low levels of atrogenes (atrogin-1, MuRF-1), which could be interpreted as an adaptive mechanism to spare muscle proteins under this catabolic condition. The loss of muscle mass was exacerbated when iota-carrageenan was administered in the joints of diabetic rats, in association with increased expression of atrogin-1, MuRF-1, and nuclear factor kappa-B. Treatment with insulin prevented the increase in atrogin-1 (TA, SO) and the loss of muscle mass (SO) in diabetic-carrageenan rats; in comparison with TA, SO muscle was more responsive to the anabolic actions of insulin. Conclusion: Acute joint inflammation overcame the adaptive mechanism in diabetic rats to prevent excessive loss of muscle mass, worsening the catabolic state. The treatment of diabetic-carrageenan rats with insulin prevented the loss of skeletal muscle mass mainly via atrogin-1 inhibition. Under the condition of DM and inflammation, muscles with the prevalence of slow-twitch, type 1 fibers were more responsive to insulin treatment, recovering the ability to grow. (AU) | |
| FAPESP's process: | 10/00892-0 - Effect of acute ankle inflammation on histological features, gene expression and levels of creatine kinase and antioxidant enzymes in the soleus and anterior tibialis muscles of diabetic rats |
| Grantee: | Iguatemy Lourenço Brunetti |
| Support Opportunities: | Regular Research Grants |