Decreased insulin responsiveness in fat cells rendered protein kinase C-deficient by a treatment with a phorbol ester.
Insulin stimulation of 2-deoxyglucose transport and lipogenesis from glucose was examined in fat cells in which protein kinase C had been down-modulated by a 3 h pretreatment with 5 X 10(-7) M 4 beta-phorbol 12 beta-myristate, 13 alpha-acetate (PMA). As compared to control fat cells, the down-modulated cells exhibited a 55-65% decrease in insulin responsiveness with no change in either the hormone sensitivity or the insulin receptor affinity. The present study shows that fat cells made protein kinase C-deficient by chronic treatment with PMA exhibit an insulin-resistant state, distal to the initial step of hormone binding.
D000273:Adipose Tissue / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D003847:Deoxyglucose / Q000378:metabolism; D007328:Insulin / Q000494:pharmacology*; D007333:Insulin Resistance; D008055:Lipids / Q000096:biosynthesis; D008297:Male; D011493:Protein Kinase C / Q000502:physiology*; D051381:Rats; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology*
D007328:Insulin; D008055:Lipids; D003847:Deoxyglucose; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate