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J. Biol. Chem., Vol. 276, Issue 19, 15688-15695, May 11, 2001
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From the Department of Medicine, Division of Endocrinology and
Metabolism, University of California, San Diego, La Jolla,
California 92093-0673, the Whittier Institute for Diabetes, La Jolla,
California 92037 and the San Diego Veterans Administration Medical
Center, San Diego, California 92161
We examined the role of heterotrimeric G protein
signaling components in insulin and insulin-like growth factor I
(IGF-I) action. In HIRcB cells and in 3T3L1 adipocytes, treatment with the G
Insulin and Insulin-like Growth Factor I Receptors
Utilize Different G Protein Signaling Components*
i inhibitor (pertussis toxin) or
microinjection of the G
inhibitor (glutathione
S-transferase-ARK) inhibited IGF-I and lysophosphatidic
acid-stimulated mitogenesis but had no effect on epidermal growth
factor (EGF) or insulin action. In basal state, Gi and
G were associated with the IGF-I receptor (IGF-IR), and after ligand
stimulation the association of IGF-IR with Gi increased concomitantly with a decrease in G association. No association of
Gi was found with either the insulin or EGF receptor.
Microinjection of anti--arrestin-1 antibody specifically inhibited
IGF-I mitogenic action but had no effect on EGF or insulin action.
-Arrestin-1 was associated with the receptors for IGF-I, insulin,
and EGF in a ligand-dependent manner. We demonstrated that
Gi, subunits, and -arrestin-1 all play a
critical role in IGF-I mitogenic signaling. In contrast, neither
metabolic, such as GLUT4 translocation, nor mitogenic signaling by
insulin is dependent on these protein components. These results suggest
that insulin receptors and IGF-IRs can function as G protein-coupled
receptors and engage different G protein partners for downstream signaling.
*
This work was supported in part by National Institutes of
Health Grant DK 33651 and by the Whittier Institute for Diabetes.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Medicine
(0673), University of California, San Diego, 9500 Gilman Dr., La Jolla,
CA 92093-0673. Tel.: 858-534-6651; Fax: 858-534-6653.
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