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Arachidonic acid and protein synthesis inhibitor act synergistically to suppress insulin‐stimulated glucose transport in 3T3‐L1 adipocytes
Author(s) -
Liu David,
Chen ChihChiun,
Chai ShinPei,
Ho LowTone,
Fong Jim C.
Publication year - 1998
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216549800204212
Subject(s) - cycloheximide , glut4 , glucose transporter , insulin , arachidonic acid , medicine , glucose uptake , 3t3 l1 , endocrinology , chemistry , protein synthesis inhibitor , protein biosynthesis , biochemistry , biology , adipocyte , adipose tissue , enzyme
The effect of arachidonic acid (AA) on insulin‐stimulated glucose transport by 3T3‐L1 adipocytes was examined in the presence of cycloheximide. We found that AA acted synergistically with cycloheximide to suppress insulin‐stimulated glucose transport, although it alone was without effect. Similar phenomena were observed while protein synthesis inhibitors other than cycloheximide were employed. Immunoblot analysis indicated that the increase in plasma membranes of the insulin‐regulated glucose transporter (GLUT4) in response to insulin was decreased in cells pretreated with cycloheximide for a prolonged time, while total amount of GLUT4 was not altered. Simultaneous presence of AA with cycloheximide had no further effect on the amount of GLUT4 in either total or plasma membranes. Thus the present study suggests that AA in the presence of a protein synthesis inhibitor seems to decrease the intrinsic activity of GLUT4.