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Volume 270,
Number 13,
Issue of March 31, 1995 pp. 7724-7730
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
Thiazolidine
Derivatives Ameliorate High Glucose-induced Insulin Resistance via the
Normalization of Protein-tyrosine Phosphatase Activities
(Received for publication, May 23, 1994; and in revised form, December 12, 1994 )
Hiroshi
Maegawa ,
Rie
Ide,
Masaaki
Hasegawa ,
Satoshi
Ugi,
Katsuya
Egawa ,
Masanori
Iwanishi,
Ryuichi
Kikkawa ,
Yukio
Shigeta,
Atsunori
Kashiwagi
The mechanisms for the insulin resistance induced by
hyperglycemia were investigated by studying the effect of high glucose
concentration (HG) and its modulation by thiazolidine derivatives, on
insulin signaling using Rat 1 fibroblasts expressing human insulin
receptors (HIRc). Incubating HIRc cells in 27 mMD-glucose for 4 days impaired the insulin-stimulated
phosphorylation of pp185 and receptor -subunits. Both protein
kinase C activities and phorbol dibutyrate binding to intact cells were
unchanged; however, cytosolic protein-tyrosine phosphatase (PTPase)
activity increased within 1 h prior to the impairment of insulin
receptor kinase in HG cells (Maegawa, H., Tachikawa-Ide, R., Ugi, S.,
Iwanishi, M., Egawa, K., Kikkawa, R., Shigeta, Y., and Kashiwagi,
A.(1993) Biochem. Biophys. Res. Commun. 197, 1078-1082).
Increased PTPase activity was consistent with a 2-fold increase in the
amount of PTP1B, and anti-PTP1B antibody inhibited this increment of
cytosolic PTPase activity in HG cells. Co-incubating cells with
pioglitazone prevented these abnormalities in cytosolic PTPase, the
PTP1B content and the impaired phosphorylation of pp185 and receptor
subunits in HG cells. Finally, HG cells had impaired
insulin-stimulated -aminoisobutyric acid uptake, which was
ameliorated by exposure to thiazolidine derivatives. In conclusion,
exposing cells to high glucose levels desensitizes insulin receptor
function, and thiazolidine derivatives can reverse the process via the
normalization of cytosolic PTPase, but not of protein kinase C.

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Copyright © 1995 by the American Society for Biochemistry and Molecular Biology.
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