Research Article| Volume 53, ISSUE 3, P382-387, March 2004

Insulin resistance and GLUT-4 glucose transporter in adipocytes from hypertensive rats

  • Gladys E Chiappe De Cingolani
    Address reprint requests to Gladys E. Chiappe de Cingolani, PhD, Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Calle 60 y 120, 1900 La Plata, Argentina
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina
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  • Claudia I Caldiz
    Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina
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  • Author Footnotes
    1 G.E.C. is an established Investigator of Consejo Nacional de Investigaciones Cientı́ficas y Técnicas (CONICET), Argentina.


      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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