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Am J Physiol Endocrinol Metab (August 8, 2006). doi:10.1152/ajpendo.00178.2006
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Submitted on April 13, 2006
Accepted on August 3, 2006

Inactivation of PKC{theta} Leads to Increased Susceptibility to Obesity and Dietary Insulin Resistance in Mice

Zhanguo Gao1, Zhong Q Wang2, Xiaoying Zhang3, Andrew A Butler4, Aamir Zuberi5, Barbara Gawronska-Kozak6, Michael Lefevre7, David A. York8, Eric Ravussin9, Hans-Rudolf Berthoud10, Owen P. McGuinness11, William T. Cefalu12, and Jianping Ye13*

1 Gene Regulation, PBRC, Baton Rouge, Louisiana, United States
2 Diabetes, PBRC, Baton Rouge, Louisiana, United States
3 Lipid protein, PBRC, Baton Rouge, Louisiana, United States
4 Neurobiology, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States
5 Functional Genomics Laboratory, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States
6 Stem Cell, PBRC, Baton Rouge, Louisiana, United States
7 PBRC, United States; Lipid protein, PBRC, Baton Rouge, Louisiana, United States
8 Pennington Biomedical Research Center, Louisiana State University, Baton Rouge,, Louisiana, United States
9 Health and Performance Enhancement Division, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States
10 Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana, United States
11 Department of Molecular Physiology & Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee, United States
12 Division of Nutrition and Chronic Diseases, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States
13 Gene Regulation Lab, Pennington Biomedical Research Center, Baton Rouge, Louisiana, United States

* To whom correspondence should be addressed. E-mail: yej{at}pbrc.edu.

In this study, we investigated the metabolic phenotype of protein kinase C theta (PKC{theta}) knockout mice (C57BL/6J) on chow diet and high fat diet (HFD). The knockout (KO) mice are normal in growth and reproduction. On chow diet, body weight and food intake were not changed in the KO mice, however body fat content was increased with corresponding decrease in body lean mass. Energy expenditure and spontaneous physical activity were decreased in the KO mice. On HFD, energy expenditure and physical activity remained low in the KO mice. The body weight and fat content were increased rapidly in the KO mice. At eight weeks on HFD, severe insulin resistance was detected in the KO mice with hyperinsulinemic-euglycemic clamp and insulin tolerance test. Insulin action in both hepatic and peripheral tissues was reduced in the KO mice. Plamsa FFA was increased and expression of adiponectin in the adipose tissue was decreased in the KO mice on HFD. This study suggests that loss of PKC{theta} reduces energy expenditure, and increases the risk of dietary obesity and insulin resistance in mice.






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