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Habegger, K.M.* ; Matzke, D.* ; Ottaway, N.* ; Hembree, J.* ; Holland, J.* ; Raver, C.* ; Mansfeld, J.* ; Müller, T.D. ; Perez-Tilve, D.* ; Pfluger, P.T. ; Lee, S. J.* ; Diaz-Meco, M.* ; Moscat, J.* ; Leitges, M.* ; Tschöp, M.H. ; Hofmann, S.M.

Role of adipose and hepatic atypical protein kinase C lambda (PKCλ) in the development of obesity and glucose intolerance.

Adipocyte 1, 203-214 (2012)
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PKCl, an atypical member of the multifunctional protein kinase C family, has been implicated in the regulation of insulinstimulated glucose transport and of the intracellular immune response. To further elucidate the role of this cellular regulator in diet-induced obesity and insulin resistance, we generated both liver (PKC-Alb) and adipose tissue (PKC-Ap2) specific knockout mice. Body weight, fat mass, food intake, glucose homeostasis and energy expenditure were evaluated in mice maintained on either chow or high fat diet (HFD). Ablation of PKCl from the adipose tissue resulted in mice that were indistinguishable from their wild-type littermates. However, PKC-Alb mice were resistant to diet-induced obesity (DIO). Surprisingly this DIO resistance was not associated with either a reduction in caloric intake or an increase in energy expenditure as compared with their wild-type littermates. Furthermore, these mice displayed an improvement in glucose tolerance. When maintained on chow diet, these mice were similar to wild types in respect to body weight and fat mass, yet insulin sensitivity was impaired compared with wt littermates. Taken together these data suggest that hepatic PKCl is modulating insulin-mediated glucose turnover and response to high fat diet feeding, thus offering a deeper understanding of an important target for anti-obesity therapeutics.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter atypical protein kinase C-lambda, diet induced obesity, energy expenditure, insulin resistance, glucose tolerance
ISSN (print) / ISBN 2162-3945
e-ISSN 2162-397X
Zeitschrift Adipocyte
Quellenangaben Band: 1, Heft: 4, Seiten: 203-214 Artikelnummer: , Supplement: ,
Verlag Landes Bioscience
Begutachtungsstatus Peer reviewed