REVIEW: Protein Kinase Czeta and Glucose Uptake

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Li-Zhong Liu^#, Ai-Bin He^#, Xiao-Jun Liu, Yi Li, Yong-Sheng Chang^*, and Fu-De Fang^*

National Laboratory of Medical Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100005, China; fax: +86-10-65253005; E-mail: fangfd@vip.sina.com

^# Co-first authors.
^* To whom correspondence should be addressed.

Received October 24, 2005; Revision received January 19, 2006

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Protein kinase Czeta (PKCzeta) is a member of the PKC family, serving downstream of insulin receptor and phosphatidylinositol (PI) 3-kinase. Many evidences suggest that PKCzeta plays a very important role in activating glucose transport response. Not only insulin but also glucose and exercise can activate PKCzeta through diverse pathways. PKCzeta activation and activity are impaired with insulin resistance in muscle and adipose tissues of type II diabetes individuals, but heightened in liver tissue, wherein it also increases lipid synthesis mediated by SREBP-1c (sterol-regulatory element-binding protein). Many studies have focused on linkage between PKCzeta and GLUT4 translocation and activation. Exploring the molecular mechanisms and pathways by which PKCzeta mediates glucose transport will highlight the insulin-signaling pathway.

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KEY WORDS: PKCzeta, GLUT4, glucose uptake

DOI: 10.1134/S0006297906070017

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