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IGF‐1 receptor as an alternative receptor for metabolic signaling in insulin receptor‐deficient muscle cells
Author(s) -
Baudry A.,
Lamothe B.,
Bucchini D.,
Jami J.,
Montarras D.,
Pinset C.,
Joshi R.L.
Publication year - 2001
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)02435-2
Subject(s) - myogenesis , myod , myogenin , insulin receptor , insulin like growth factor 1 receptor , glycogen synthase , biology , endocrinology , myocyte , medicine , receptor , signal transduction , insulin , chemistry , microbiology and biotechnology , biochemistry , insulin resistance , growth factor
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 125 I‐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.