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J. Biol. Chem., Vol. 276, Issue 18, 15292-15297, May 4, 2001
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From the Department of Physiology and Biophysics, The University of
Iowa, Iowa City, Iowa 52242
Various studies have demonstrated that the
platelet-derived growth factor (PDGF) receptor in adipocytes can
activate PI 3-kinase activity without affecting insulin-responsive
glucose transporter (GLUT4) translocation. To investigate this
phenomenon of receptor signaling specificity, we utilized single cell
analysis to determine the cellular distribution and signaling
properties of PDGF and insulin in differentiated 3T3L1 adipocytes. The
insulin receptor was highly expressed in a large percentage of the cell
population (>95%) that also expressed caveolin 2 and GLUT4 with very
low levels of the PDGF receptor. In contrast, the PDGF receptor was only expressed in ~10% of the differentiated 3T3L1 cell population with relatively low levels of the insulin receptor, caveolin 2, and
GLUT4. Consistent with this observation, insulin stimulated the
phosphorylation of Akt in the caveolin 2- and GLUT4-positive cells, whereas PDGF primarily stimulated Akt phosphorylation in the
caveolin 2- and GLUT4-negative cell population. Furthermore, transfection of the PDGF receptor in the insulin receptor-, GLUT4-, and
caveolin 2-positive cells resulted in the ability of PDGF to stimulate
GLUT4 translocation. These data demonstrate that differentiated 3T3L1
adipocytes are not a homogeneous population of cells, and the lack of
PDGF receptor expression in the GLUT4-positive cell population accounts
for the inability of the endogenous PDGF receptor to activate GLUT4 translocation.
Differentiated 3T3L1 Adipocytes Are Composed of
Heterogenous Cell Populations with Distinct Receptor Tyrosine Kinase
Signaling Properties*
,
*
This work was supported by National Institutes of Health
Grants DK33823 and DK25295.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.
Supported by a mentor-based postdoctoral fellowship from the
American Diabetes Association.
§
To whom all correspondence should be addressed. Tel.: 319-335-7823;
Fax: 319-335-7886; E-mail: Jeffrey-Pessin@uiowa.edu.
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