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© Research
Publication : FEBS letters

IGF-1 receptor as an alternative receptor for metabolic signaling in insulin receptor-deficient muscle cells

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in FEBS letters - 19 Jan 2001

Baudry A, Lamothe B, Bucchini D, Jami J, Montarras D, Pinset C, Joshi RL

Link to Pubmed [PMID] – 11163767

FEBS Lett. 2001 Jan;488(3):174-8

We have derived skeletal muscle cell lines from wild-type (wt) and insulin receptor (IR) knockout mice to unravel the metabolic potential of IGF-1 receptor (IGF-1R). Both wt and IR(-/-) myoblasts differentiated into myotubes with similar patterns of expression of muscle-specific genes such as MyoD, myogenin and MLC1A indicating that IR is not required for this process. Binding of 125I-IGF-1 on wt and IR(-/-) myotubes was similar showing that IGF-1R was not upregulated in the absence of IR. Stimulation of IR(-/-) myotubes with IGF-1 (10(-10) to 10(-7) M) increased glucose uptake and incorporation into glycogen, induced IRS-1 phosphorylation and activated PI 3-kinase and MAP kinase, two enzymes of major signaling pathways. These effects were comparable to those obtained with wt myotubes using insulin or IGF-1 or with IR(-/-) myotubes using insulin at higher concentrations. This study provides a direct evidence that IGF-1R can represent an alternative receptor for metabolic signaling in muscle cells.

http://www.ncbi.nlm.nih.gov/pubmed/11163767