Insulin Resistance and the Alterations of Glucose Transporter‐4 in Adipose Cells From Cachectic Tumor‐Bearing Rats

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Abstract
Background: Insulin resistance may play an important role in cancer cachexia; however, its mechanisms remain to be clarified. Methods: Cellular mechanisms of insulin resistance in tumor-bearing rats (TBR) were investigated in isolated adipose cells by measuring 3-O-[14C]methyl glucose transport activity and glucose transporter-4 (GLUT4) protein in low-density microsomes at a basal state and in the plasma membrane at an insulin-stimulated state. Results: The insulin-stimulated glucose transport activity in adipose cells from TBR was significantly lower than that of control rats (CTR) (0.51 ± 0.25 and 2.27 ± 0.11 fmol/cell/min, respectively). The amount of GLUT4 in low-density microsomes at a basal state and in plasma membrane at an insulin-stimulated state was less in TBR than in CTR. Conclusions: These data suggest that the insulin resistance seen in the adipose cells of these tumor-bearing rats was caused in part by both a decreased amount of GLUT4 protein in a basal state and a decreased translocation of GLUT4 in response to insulin stimulation. (Journal of Parenteral and Enteral Nutrition 21:347–349, 1997)