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 (PKCβ) in energy homeostasis. This review highlights recent findings on the role of PKCβ
activation in the genesis and progression of obesity, and of PKCβ repression in mediating the beneficial effects
of physical exercise. Available data support a model in which adipose PKCβ activation is among the initiating
events that disrupt mitochondrial function through interaction with p66shc and amplify fat accumulation and
adipose dysfunction, with systemic consequences. Manipulation of PKCβ levels, activity, or signaling could provide
a therapeutic approach to combat obesity and associated metabolic disorders.
© 201