Palmitate stimulates glucose transport in rat adipocytes by a mechanism involving translocation of the insulin sensitive glucose transporter (GLUT4)

Robert W. Hardy, Jack H. Ladenson, Erik J Henriksen, John O. Holloszy, Jay M. McDonald

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)343-349
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume177
Issue number1
DOIs
StatePublished - May 31 1991

Fingerprint

Facilitative Glucose Transport Proteins
Palmitates
Adipocytes
Rats
Insulin
Glucose
Muscle
Muscles
Sphingosine
Staurosporine
Protein C Inhibitor
Deoxyglucose
Cell membranes
Protein Kinase Inhibitors
Microsomes
Protein Kinase C
Fatty Acids
Cell Membrane
Tissue

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Palmitate stimulates glucose transport in rat adipocytes by a mechanism involving translocation of the insulin sensitive glucose transporter (GLUT4). / Hardy, Robert W.; Ladenson, Jack H.; Henriksen, Erik J; Holloszy, John O.; McDonald, Jay M.

In: Biochemical and Biophysical Research Communications, Vol. 177, No. 1, 31.05.1991, p. 343-349.

Research output: Contribution to journalArticle

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