forms of obesity will assist us in designing more effective therapies and in identifying high-risk individuals for early intervention. Several lines of evidence have emerged regarding the potential role of protein kinase C-beta (PKCβ) in controlling energy homeostasis. Metabolic stress caused by diet-induced or genetic-related obesity results in the activation of PKCβ in an adipose- and isoform-specific manner. This review focuses on the role of adipose PKCβ activation in the pathogenesis of obesity, and describes recent evidence suggesting that the PKCβ–mitochondrial axis provides a link between nutrient overload and adipose dysfunction