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Protein kinase C-beta: An emerging connection between nutrient excess and obesity

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ELSEVIER
DOI: 10.1016/j.bbalip.2014.07.011

Keywords

Obesity; PKC beta; Mitochondria; Adipose dysfunction; Signal transduction

Funding

  1. NIH [79091]

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There is currently a global epidemic of obesity as a result of recent changes in lifestyle. Excess body fat deposition is caused by an imbalance between energy intake and energy expenditure due to interactions between genetic and environmental factors. The signals and biological mechanisms that trigger fat accumulation by disrupting energy homeostasis are not well understood. There is considerable evidence now supporting a possible role of protein kinase C beta (PKC beta) in energy homeostasis. This review highlights recent findings on the role of PKC beta activation in the genesis and progression of obesity, and of PKC beta repression in mediating the beneficial effects of physical exercise. Available data support a model in which adipose PKC beta activation is among the initiating events that disrupt mitochondrial function through interaction with p66(shc) and amplify fat accumulation and adipose dysfunction, with systemic consequences. Manipulation of PKC beta levels, activity, or signaling could provide a therapeutic approach to combat obesity and associated metabolic disorders. (C) 2014 Published by Elsevier B.V.

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