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Protein Kinase CbetaI Interacts With the beta1-adrenergic Signaling Pathway to Attenuate Lipolysis in Rat Adipocytes

Protein Kinase CbetaI Interacts With the beta1-adrenergic Signaling Pathway to Attenuate Lipolysis in Rat Adipocytes

Jiro Nakamura

Biochim Biophys Acta. 2008 May;1781(5):277-81.

PMID: 18440322

Abstract:

We have shown previously that insulin attenuates beta1-adrenergic receptor (beta1-AR)-mediated lipolysis via activation of protein kinase C (PKC) in rat adipocytes. This antilipolysis persists after removal of insulin and is independent of the phosphodiesterase 3B activity, and phorbol 12-myristate 13-acetate (PMA) could substitute for insulin to produce the same effect. Here, we attempted to identify the PKC isoform responsible for antilipolysis. Isolated adipocytes were treated with high and low concentrations of PMA for up to 6 h to degrade specific PKC isoforms. In the PMA-treated cells, the downregulation profiles of PKC isoforms alpha and betaI, but not betaII, delta, epsilon, or zeta, correlated well with a decrease of lipolysis-attenuating effect of PMA. After rats fasted for 24 h, adipocyte expression of PKC isoform alpha increased, while expression of PKCdelta decreased. Fasting did not change the potency of PMA to attenuate lipolysis, however. The lipolysis-attenuating effect of PMA was blocked by the PKCbetaI/betaII inhibitor LY 333531, but not by the PKCbetaII inhibitor CGP 53353 or the PKCdelta inhibitor rottlerin. These data suggest that PKCbetaI interacts with beta1-AR signaling and attenuates lipolysis in rat adipocytes.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP145915602-A	CGP-53353		145915-60-2	Price
IAR42411914	Protein Kinase CβI isozyme human			Price

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