Modulating role of dietary fat, energy
restriction, and the effect of age on the
expression of proliferating cell nuclear
antigen and protein kinase C activity
in prostate glands of rats
Kaiqi Yao, Cathy M. Lasko, and Ranjana P. Bird
Department of Foods and Nutrition, University of Manitoba, Winnipeg, Manitoba, R3T 2N2 Canada
The present study investigated the role of dietary fat and energy restriction (ER) on the proliferative status and
the protein kinase c (PKC) activity in the prostate glands in young (3-week-old, n ϭ 40) and adult rats
(10-week-old, n ϭ 40). F344 male rats, young and adult, were allocated to four dietary groups (n ϭ 10/group):
high fat (23% wt/wt) or low fat (5% w/w) ad libitum (HFAL or LFAL) and high- or low-fat energy restriction
(HFER or LFER). Energy-restricted rats were fed 80% of the energy intake of the ad libitum fed rats. After 12
weeks of feeding, the proliferating cell nuclear antigen (PCNA) labeling index in prostate glands was higher in
young rats than in adult rats. Both the HFAL and LFAL groups had higher PCNA labeling index than both the
HFER and LFER groups in each age group. In addition, the HFAL group had higher PCNA labeling index than
the LFAL group. Dietary fat and ER markedly affected the PKC activity, which decreased in the order HFAL Ͼ
HFER ϭ LFAL Ͼ LFER for both young and adult animals. The effect of high-fat diet and ER were more evident
in the younger animals than in the adult animals. Among the young animals, the absolute total PKC activity was
higher (P Յ 0.05) in the high-fat groups than in the low-fat groups and a higher proportion of the total PKC was
associated with the membrane fraction. In both young and adult rats, ER decreased the total PKC activity and
the ratio of PKC activity in the cytosol to the membrane fractions compared with the ad lib counterparts. We
conclude that age, a high-fat diet, and energy restriction modulate PCNA expression and the PKC activity of
prostatic tissue. (J. Nutr. Biochem. 9:236–241, 1998) © Elsevier Science Inc. 1998
Keywords: prostate glands; protein kinase C; proliferating cell nuclear antigen; energy restriction; dietary fat
Introduction
Dietary lipids and energy are well established modulators of
cell growth and differentiation including signal transduction
and gene expression.
1–5
Evidence supports the role of
dietary lipids and/or energy as a modulator of carcinogen-
esis in several organs.
4–12
Growth of the prostate glands is
dependent on the hormonal state of the animals which in
turn depends on the nutritional status and the age of the
animals. Epidemiologic and animal studies have provided
evidence in support of the conjecture that dietary fat and
energy exert a profound effect on the carcinogenic process
in the prostate glands.
4–13
The exact mechanism by which
the high-fat diet exerts these effects is poorly understood.
Postulations are that dietary factors may affect the promo-
tional steps of prostate cancer development.
Animal models provide the opportunity to test and refine
hypotheses linking diet in the etiology and prevention of
different types of cancer. Unfortunately, attempts to develop
animal models to study prostate cancer have met with only
limited success. Considering that the susceptibility of an
organ to carcinogenesis may depend on the growth and
hormonal status of a particular organ, it is important to
determine the effect of dietary lipid and energy restriction
on the growth of normal prostate glands.
The main objective of the present investigation was to
assess the effect of dietary fat and energy restriction on the
Address correspondence and reprint requests to Dr. Ranjana P. Bird,
Department of Foods and Nutrition, University of Manitoba, Winnipeg,
Manitoba R3T 2N2 Canada.
Received December 5, 1996; accepted November 11, 1997.
Nutritional Biochemistry 9:236–241, 1998
© Elsevier Science Inc. 1998 0955-2863/98/$19.00
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