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Inactivation of PKC leads to increased susceptibility to obesity and dietary insulin resistance in mice

¹Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, Louisiana; ²Center for Advanced Nutrition, Utah State University, Logan, Utah; and ³Department of Molecular Physiology and Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee

Submitted 13 April 2006 ; accepted in final form 3 August 2006

In this study, we investigated the metabolic phenotype of PKC knockout mice (C57BL/6J) on chow diet and high-fat diet (HFD). The knockout (KO) mice are normal in growth and reproduction. On the chow diet, body weight and food intake were not changed in the KO mice; however, body fat content was increased with a 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 8 wk 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 free fatty acid 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 reduces energy expenditure and increases the risk of dietary obesity and insulin resistance in mice.

protein kinase C; dietary obesity; insulin resistance

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