Neonatal intramuscular injection of plasmid DNA encoding GLP-1 reduces serum insulin level and modifies skeletal muscle myosin heavy chain composition in adult rats

Title:

Neonatal intramuscular injection of plasmid DNA encoding GLP-1 reduces serum insulin level and modifies skeletal muscle myosin heavy chain composition in adult rats

Creator:

Wang, L., Guo, F., Wei, S., and Zhao, R.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:f974a423-d377-4501-92ce-be85fda727cc
uuid:f974a423-d377-4501-92ce-be85fda727cc

Subject:

Fyziologie člověka a srovnávací fyziologie, inzulin, insulin, GLP-1, suckling, skeletal muscle, myosin heavy chain (MyHC), 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print

Description:

To test the hypothesis that neonatal GLP-1 exposure may program myosin heavy chain (MyHC) composition in adult skeletal muscle, two-day-old rats were transfected intramuscularly with vacant vector plasmid (VP), or recombinant plasmid expressing secretory GLP-1 at the doses of 60 μg (LG) and 120 μg (HG), respectively. Expression of GLP-1 mRNA was detected in muscles of both LG and HG rats 7 days after transfection, with more abundant GLP-1 transcript seen in LG rats. In accordance with the GLP-1 expression, LG rats demonstrated more significant responses to neonatal GLP-1 exposure. Small yet significant growth retardation was observed in LG rats, which is accompanied with significantly reduced serum insulin concentration at 8 weeks of age compared to VP rats. The responses of skeletal muscle were dependent on muscle type. Significant increase of PGC-1α and GLUT4 mRNA expression was detected in soleus of LG rats, whereas a MyHC type switch from ⅡB to Ⅰ was seen in gastrocnemius. These results indicate that neonatal exposure of healthy pups to ectopic GLP-1 causes growth retardation with decreased serum insulin as well as muscle type-dependent modifications in MyHC type composition and metabolic gene expression in adult rats., L. Wang ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

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

Source:

Physiological research | 2010 Volume:59 | Number:4

Harvested from:

CDK

Metadata only:

false