Studies on the mechanism of dietary fat and energy modulation of skin carcinogenesis
suggest that these diets may act through the cellular binding site of the phorbol ester tumor
promoters, protein kinase C (PKC). High-fat diets increase the activity of PKC but have no
impact on the steady-state protein levels. Energy restriction reduces the activity of PKC,
presumably through reduction in the steady-state levels of particular isoenzymes (PKC α
and PKC ζ). Phorbol-binding studies with epidermal cells from mice fed energy-restricted …