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J. Biol. Chem., Vol. 277, Issue 6, 3809-3812, February 8, 2002
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From the Preincubation of 3T3-L1 adipocytes in
high glucose or glucosamine decreases acute insulin (100 nM)-stimulated glucose transport provided that
insulin (0.6 nM) is included during preincubation. GLUT4
expression is unchanged (Nelson, B. A., Robinson, K. A., and
Buse, M. G. (2000) Diabetes 49, 981-991).
Munc18-c, a Syntaxin 4-binding protein, is a proposed regulator
of the docking/fusion of GLUT4-containing vesicles with the plasma
membrane. We examined the subcellular distribution of Munc18-c in
response to acute (15-min) insulin (100 nM) stimulation
after preincubation in 5 or 25 mM glucose ± 0.6 nM insulin. Immunoblotting detected Munc18-c mainly in the
Triton X-100-soluble plasma membrane (TS-PM) and the Triton
X-100-insoluble low density microsomal (TI-LDM) fraction. Under each
condition except high glucose + insulin preincubation, acute insulin
increased Munc18-c (~50-200%) in TS-PM and decreased Munc18-c
(~60%) in TI-LDM. Munc18-c traffic was time-dependent with a lag time of ~3 min compared with GLUT4. Preincubation with high glucose + 0.6 nM insulin significantly impaired acute
insulin-stimulated Munc18-c trafficking and decreased basal Munc18-c in
the TI-LDM. Preincubation with glucosamine + insulin had similar
effects. Total cellular Munc18-c remained unchanged. In conclusion,
acute insulin stimulation promotes the translocation of
Munc18-c, apparently from a TI-LDM-associated compartment to the TS-PM.
Chronically increased glucose flux or exposure to glucosamine disrupts
this process, which may negatively impact the fusion of
GLUT4-containing vesicles with the plasma membrane.
ACCELERATED PUBLICATION
Insulin Acutely Regulates Munc18-c Subcellular Trafficking
ALTERED RESPONSE IN INSULIN-RESISTANT 3T3-L1 ADIPOCYTES*
§,, and¶
Department of Medicine, Division of
Endocrinology, Diabetes and Medical Genetics and the ¶ Department
of Biochemistry/Molecular Biology, Medical University of South
Carolina, Charleston, South Carolina 29425
*
This work was supported in part by Research Grant DK-02001
from the NIDDK, National Institutes of Health (to M. G. B.). This paper was presented in part at the 2001 National Meeting of the American Diabetes Association.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,
Endocrinology, Diabetes and Medical Genetics Division, Medical University of South Carolina, 96 Jonathan Lucas St., Ste. 323, Charleston, SC 29425. Tel.: 843-792-2529; Fax: 843-792-4114; E-mail: busemg@musc.edu.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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