PALMITATE STIMULATES GLUCOSE-TRANSPORT IN RAT ADIPOCYTES BY A MECHANISM INVOLVING TRANSLOCATION OF THE INSULIN SENSITIVE GLUCOSE TRANSPORTER (GLUT4)

被引:48
作者
HARDY, RW
LADENSON, JH
HENRIKSEN, EJ
HOLLOSZY, JO
MCDONALD, JM
机构
[1] WASHINGTON UNIV, SCH MED, DEPT PATHOL, ST LOUIS, MO 63110 USA
[2] WASHINGTON UNIV, SCH MED, DEPT MED, ST LOUIS, MO 63110 USA
[3] UNIV ARIZONA, DEPT EXERCISE & SPORT SCI, TUCSON, AZ 85721 USA
关键词
D O I
10.1016/0006-291X(91)91989-P
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
In rat adipocytes, palmitate: a) increases basal 2-deoxyglucose transport 129±27% (p<0.02), b) decreases the insulin sensitive glucose transporter (GLUT4) in low density microsomes and increases GLUT4 in plasma membranes and c) increases the activity of the insulin receptor tyrosine kinase. Palmitate-stimulated glucose transport is not additive with the effect of insulin and is not inhibited by the protein kinase C inhibitors staurosporine and sphingosine. In rat muscle, palmitate: a) does not affect basal glucose transport in either the soleus or epitrochlearis and b) inhibits insulin-stimulated glucose transport by 28% (p<0.005) in soleus but not in epitrochlearis muscle. These studies demonstrate a potentially important differential role for fatty acids in the regulation of glucose transport in different insulin target tissues. © 1991.
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收藏
页码:343 / 349
页数:7
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