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Caloric Restriction preserves replicative potential.....

ufotruth at ix.netcom.com ufotruth at ix.netcom.com
Sat Jan 16 23:04:51 EST 1999


Everyone,

This abstract is a few years old, and some of you may have already
read it before, but to me it is very interesting. It seems to me that
if cellular replicative potential, which is controled of course by
telomere length, is conserved by caloric restriction, then perhaps by
increasing cellular replicative potential (perhaps through a
telomerase inducer or vector) the same life extending effects could be
observed.

Anyway, here is the abstract....

Best Regards,
William

-----

Caloric restriction: conservation of cellular replicative capacity in
vitro accompanies life-span extension in mice.
Pendergrass WR, Li Y, Jiang D, Fei RG, Wolf NS
Exp Cell Res 1995 Apr 217:2 309-16

Abstract
We have tested whether life-long caloric restriction (CR) slows or
delays the age-related loss of cellular replicative potential that
occurs during normal aging in ad libitum (AL) fed mice. Both mean and
maximum life spans of the restricted animals (60% of AL intake) were
significantly extended 30-40% by CR treatment. Proliferative
potential, measured by determining the fraction of cells capable of
forming large clones in vitro, was compared in five cell types from
six tissue sites from two strains of mice (Male (C57BL/6 x
DBA/2)F1("B6D2F1") and female (C57BL/6 x C3H)F1("B6C3F1")). This
included four nonhematopoietic organ sites: fibroblast cells from ear
skin, tail skin, and subdermal connective tissue and epithelial cells
from the medullary part of the kidney and two cell types,
myofibroblasts and endothelial-like cells, from spleen and bone
marrow. The proliferative potential of cells from AL mice decreased
progressively with age in all tissues sites of both mouse strains. CR
delayed or decreased the loss of proliferative potential in all
situations, but the timing of this was tissue specific. For cells from
the four nonhematopoietic tissues sites from female B6C3F1 female
mice, CR delayed the onset of proliferative loss, such that the
fraction of large clones was significantly greater for the CR 18- to
24-month-old mice than in AL controls at three of four sites (as
determined by the fraction of large clones after 1 week of clonal
growth). The proliferative loss in CR tissues then accelerated from 24
to 30 months, so that both CR and AL mice had similar fractions of
large clones after 30 months of age. CR was also seen to delay loss of
proliferative potential in cells from skin and kidney of B6D2F1 male
mice at 23-24 months of age when cloned for 2 weeks. For fibroblast
and endothelial-like cells from bone marrow and spleen stromal sites
from both strains of mice, CR also significantly decreased loss of
proliferative potential; furthermore, in these tissues the
proliferative advantages remained or increased from 24 to over 30
months of age. In companion studies (N.S. Wolf et al., 1995. Exp.
Cell. Res. 217, 000-000), CR was seen to decrease age-related losses
in the maximal rates of cell replication in vivo in a panel of tissues
from B6D2F1 male mice.(ABSTRACT TRUNCATED AT 400 WORDS)






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