Insulin receptor‐deficient cells as a new tool for dissecting complex interplay in insulin and insulin‐like growth factors

FEBS Letters

Jami, J²  Christoffersen, C.T¹  De Meyts, P¹  Joshi, R.L²  Bucchini, D²  Baudry, A²  Lamothe, B² 

[1] Hagedorn Research Institute, Niels Steensens Vej 6, DK-2820 Gentofte, Denmark;Institut Cochin de Génétique Moléculaire, INSERM U257, 24, Rue du Faubourg Saint-Jacques, 75014 Paris, France

关键词: Insulin receptor;    Insulin-like growth factor 1 receptor;    Insulin action;    Signal transduction;    IGF;    insulin-like growth factor;    IGF-1R;    type 1 IGF-1 receptor;    IR;    insulin receptor;    MAP kinase;    mitogen-activated protein kinase;    PI 3-kinase;    phosphatidylinositol 3-kinase;   

DOI  :  10.1016/S0014-5793(98)00377-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Cell systems derived from knockout mice for the insulin receptor (IR) or the IGF-1 receptor (IGF-1R) represent unique tools for dissecting complex interplay in the actions of insulin and insulin-like growth factors through their cognate versus non-cognate receptor. In this study, we used a fibroblast cell line derived from IR-deficient mice to investigate metabolic and mitogenic effects of IGF-1 and insulin. IGF-1 was able to stimulate glucose uptake, glucose incorporation into glycogen and thymidine incorporation in such cells. Phosphatidylinositol 3-kinase and mitogen-activated protein kinase, two enzymes of major metabolic-mitogenic signaling pathways, were activated upon stimulating these cells with IGF-1. All these effects were also achieved when IR-deficient cells were stimulated with insulin. Thus, IGF-1R can represent an alternative receptor through which insulin might exert some of its effects.

【 授权许可】

Unknown