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Endocrinology, Vol 132, 689-692, Copyright © 1993 by Endocrine Society
ARTICLES |
ML Standaert, DR Cooper, H Hernandez, TP Arnold and RV Farese
Research Service, J. A. Haley V.A. Hospital, Tampa, Florida 33612.
In rat adipocytes, chronic incubation with 12-O-tetradecanoylphorbol-13- acetate (TPA) reduced immunoreactive protein kinase-C (PKC) beta, gamma, delta, and zeta isoforms by 40-60% and PKC alpha by 75%, but had little effect on PKC epsilon levels. In BC3H-1 myocytes, chronic TPA treatment had no effect on PKC beta, increased PKC zeta, and depleted PKC alpha. Acute treatment with insulin induced the translocation of PKC beta in the myocytes both before and after chronic TPA treatment, but had no acute effect on the alpha or zeta isoforms. In contrast, acute TPA treatment in the myocytes had little effect on PKC beta, but induced the rapid translocation of alpha and zeta. The differential effects of chronic TPA treatment on the down-regulation of PKC beta may explain why insulin continues to activate biological processes in TPA- treated BC3H-1 myocytes, but not in adipocytes.
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