<p>This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p> <p>We investigated the possible interplay between insulin
and glucose signaling pathways in rat pancreatic <italic>β</italic>-cell
with a special focus on the role of glucose in IRS signaling
<italic>in vivo</italic>. Three groups of rats were constituted by combining
simultaneous infusion during 48 h either of glucose
and/or insulin, or glucose+diazoxide: Hyperglycemic-
Hyperinsulinemic (HGHI), euglycemic-Hyperinsulinemic
(eGHI), Hyperglycemic-euinsulinemic (HGeI). Control rats
were infused with 0,9% NaCl. In HGHI and HGeI rats
plasma glucose levels were maintained at 20-22 mmol/l. In
eGHI rats, plasma glucose was not different from that of
controls, whereas plasma insulin was much higher than
in controls. In HGHI rats, IRS-2 mRNA expression, total
protein and phosphorylated protein amounts were increased
compared to controls. In HGeI rats, only IRS-2
mRNA expression was increased. No change was observed
in eGHI rats whatever the parameter considered. In all
groups, mRNA concentration of IRS-1 was similar to that
of controls. The quantity of total and phosphorylated IRS-
1 protein was dramatically increased in HGHI rats and
to a lesser extent in eGHI rats. Neither mRNA nor IRS-1
protein expression were modified in HGeI rats. The data
suggest that glucose and insulin play at once a specific
and a complementary role in islet IRSs signaling. Especially,
glucose stimulates IRS-2 mRNA expression whatever
the insulin status and independently of the secretory
process. The differential regulation of IRS-1 and
IRS-2 expressions is in agreement with their supposed different involvement in the control of <italic>β</italic>-cell growth and
function.</p>
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Exp Diabesity Res. 2004; 5(4):257-263