Carcinogenesis, Vol 18, 159-166, Copyright © 1997 by Oxford University Press
H Hikita, J Vaughan and HC Pitot
The loss of body and liver weight caused by chronic caloric restriction and
its effects on carcinogenesis are well known; however, the effects of acute
fasting on carcinogenesis have not been intensively investigated. We have
studied some parameters of rat liver during short- term fasting and its
effect on the stage of promotion in hepatocarcinogenesis in rats. During
two fasting periods, body and liver weight decreased remarkably.
Bromodeoxyuridine (BrdU) labeling indices (LI) decreased, and cell density
increased prominently in liver sections. Hematoxylin and eosin-stained and
nick end labeling (TUNEL)- stained sections showed an increase of apoptotic
bodies in the absence of necrosis during the fasting period. Moreover, gel
electrophoresis of DNA isolated from whole liver revealed ladder formation
indicative of nucleosomal DNA cleavage. At the beginning of the fasting
period livers exhibited a small but definite number of altered hepatic foci
(AHF) expressing glutathione S-transferase, placental form (GST-P), but at
the end of the fasting period no AHF were discernible in all livers of
animals subjected to the fasting period. After refeeding, cell density and
the incidence of apoptotic bodies decreased prior to a transient increase
of BrdU LI. The percentage volume of liver occupied by AHF of fasted rats
was significantly greater than that of control rats at 140 days after
initiation. These results suggest that both the liver weight loss and the
complete loss of discernible AHF from short-term fasting was caused by (i)
decrease of cell volume, (ii) cell loss by apoptosis, and (iii) a decrease
of hepatocyte proliferation. Furthermore, this relatively transient liver
weight loss enhanced the promotion of hepatocarcinogenesis, possibly by
enhanced cell proliferation compensatory to the fasting cycles.
ARTICLES
The effect of two periods of short-term fasting during the promotion stage of hepatocarcinogenesis in rats: the role of apoptosis and cell proliferation
McArdle Laboratory for Cancer Research, University of Wisconsin Medical School, Madison 53706, USA.
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