In:
Journal of Parenteral and Enteral Nutrition, Wiley, Vol. 21, No. 6 ( 1997-11), p. 347-349
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 ‐[ 14 C]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)
Type of Medium:
Online Resource
ISSN:
0148-6071
,
1941-2444
DOI:
10.1177/0148607197021006347
Language:
English
Publisher:
Wiley
Publication Date:
1997
detail.hit.zdb_id:
2170060-6