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. Author manuscript; available in PMC: 2009 Oct 2.
Published in final edited form as: Biochem J. 2008 Jul 15;413(2):315–322. doi: 10.1042/BJ20071559

Figure 5. Relationship between PKCα depletion and PKA activation in adipocytes.

Figure 5

Adrenaline (EPI; 10−5 M) increased PKA activation by 60 ± 5%, 16 h of PMA (TPA; 100 nM) treatment also stimulated PKA activation by 65 ± 2%. PKA activation was increased by 75 ± 15% following treatment with PKCα antisense (As-PKC alpha) oligomers. The results represent the means of three independent experiments done in triplicate. (B) The functional consequence of the inhibition by PKCα and adrenaline treatment. The depletion of PKCα or adrenaline treatment resulted in an increase in intracellular cAMP levels and in increased lipolysis as well as inhibition of heparin-releasable LPL activity. Intracellular cAMP concentration was measured in cell lysates using an enzyme immunoassay as described in the Experimental section. Change in lipolysis was measured by quantifing glycerol released into the medium, also as described in the Experimental section. LPL activity is expressed as nmol of FFA released/h per mg of protein. The results represent the means of four independent experiments. *P < 0.01, **P < 0.05 compared with the untreated control.