Abstract
To investigate the mechanisms that cause insulin resistance in hypertension, experiments
were performed to study the effect of insulin on glucose transport, GLUT-4 translocation
from intracellular to plasma membranes and GLUT-4 phosphorylation in isolated adipocytes
from normotensive Wistar (W) and spontaneously hypertensive rats (SHR). Glucose transport
was measured in adipocytes incubated with 3-O-d[Methyl-3H] glucose with and without insulin (0.1 to 5 nmol/L). GLUT-4 protein was determined
by Western blot immunoanalysis with GLUT-4 antibody. Phosphorylation of GLUT-4 was
measured by immunoprecipitation with GLUT-4 antibody followed by immunoanalysis with
phosphoserine or phosphothreonine antibodies. Compared with adipocytes from W, insulin-stimulated
glucose transport was lower in the SHR (P < .05). GLUT-4 protein expression was similar in adipocytes from W and SHR. Insulin
increased GLUT-4 translocation from intracellular to plasma membranes in both groups.
This effect was lower in the SHR (P < .05). The effect of insulin on GLUT-4 serine phosphorylation showed no changes
in plasma membranes from W and decreased in the SHR (P < .05). In intracellular membranes, insulin increased specific GLUT-4 serine phosphorylation
in both groups (P < .05), but the increase was lower in the SHR (P < .05). The results suggest that a deficient GLUT-4 translocation to plasma membranes
in response to insulin shown in adipocytes from SHR, which was accompanied by a decrease
in GLUT-4 phosphorylation at serine site, could be one of the causes of insulin resistance
in hypertension.
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Article info
Publication history
Accepted:
October 25,
2003
Received:
July 2,
2003
Identification
Copyright
© 2004 Elsevier Inc. Published by Elsevier Inc. All rights reserved.