DIETARY ENERGY RESTRICTION-INDUCED MODULATION OF PROTEIN-KINASE-C-ZETA ISOZYME IN THE HAMSTER PANCREAS

Dietary restriction in experimental animals enhances life span, delays disease, inhibits immunological perturbations, and ameliorates cancer . Protein kinase C (PKC) isozymes mediate signals generated by hormone s, growth factors, and neurotransmitters for cell proliferation and di fferentiation. The results of our study showed that a C-terminally dir ected anti-PKC zeta antibody detected an 81-kDa band in the pancreases of control and energy-restricted hamsters. Syrian golden hamsters wer e fed energy-restricted diets formulated such that the hamsters receiv ed 90% (10% energy restriction (ER)), 80% (20% ER), or 60% (40% ER) of the total energy consumed by control hamsters, with the energy reduce d proportionally from fat and carbohydrate. ER decreased PKC zeta isoz yme levels by 40-75% in hamsters fed 10, 20, and 40% ER diets for 8 wk . PKC zeta isozyme expression was decreased by 75-80% in hamsters fed ER diets for 15 wk. Although ER caused significant decreases in PKC ze ta isozyme levels compared with those of control hamsters at both time points, the relative differences in PKC zeta levels between the dieta ry ER groups (10, 20, and 40%) were small and not significant. A signi ficant decrease in the body weights of ER animals compared with those of controls was observed at both time points. No differences in tomato lectin and phytohemagglutinin reactivity were observed between contro l animals and animals fed 10, 20, and 40% ER diets. Furthermore, the c ellular expression of PKC zeta in the hamster pancreas did not differ among hamsters fed the various ER diets. These observations may be imp ortant for understanding not only the role of dietary ER in pancreatic cancers but also PKC zeta signal transduction mechanisms in normal pa ncreatic physiology. (C) 1995 Wiley-Liss, Inc.