Abstract
Protein kinase C activity has been identified in the rat brown adipocyte. About 60% of this activity is found in the cytosolic fraction under basal conditions, and 12-O-tetradecanoylphorbol 13-acetate (TPA) causes a rapid shift from the cytosol to the particulate fraction. Norepinephrine and phenylephrine cause a similar redistribution that can be blocked by prazosin but not by alprenolol. alpha 1-Adrenergic agonists cause three- to fivefold stimulation of type 2 iodothyronine 5'-deiodinase activity in brown adipocytes. TPA has no effect on basal deiodinase activity and reduces the response of the enzyme to alpha 1-adrenergic agonists. These results suggest that the translocation of protein kinase C from cytosol to particulate fraction is not sufficient to increase deiodinase activity but can modulate the alpha 1-adrenergic agonist-mediated responses in these cells.
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