Re: more about growth hormone and the decline of years

Date: Wed Feb 06 2002 - 19:27:21 MST

In a message dated 2/6/02 5:33:19 PM, writes:

>GH bad for you?
>well I guess we should find something to block it then!!
>oh wait.. then we'll be obese and have no immune function and cant heal

Obese, yes, but the other effects appear less significant than aging.
Would you rather be thin and die at 80 or fat and die at 112? I like
being thin, but not *that* much.
Here's a cite:

Flurkey, Kevin; Papaconstantinou, John; Miller, Richard A.; Harrison, David
E.. Lifespan extension and delayed immune and collagen aging in mutant mice
with defects in growth hormone production. In: Proceedings of the National
of Sciences of the United States of America June 5, 2001. 98 (12): 6736-6741.
Language: English; Pub type: JOURNAL ARTICLE

Abstract: Single-gene mutations that extend lifespan provide valuable tools
for the
exploration of the molecular basis for age-related changes in cell and tissue
function and for
the pathophysiology of age-dependent diseases. We show here that mice h
omozygous for
loss-of-function mutations at the Pit1 (Snell dwarf) locus show a >40%
increase in mean and
maximal longevity on the relatively long-lived (C3H/HeJXDW/J)F1 background.
 dwJ/dw animals show delays in age-dependent collagen cross-linking and in six
age-sensitive indices of immune system status. These findings thus
demonstrate that a single
gene can control maximum lifespan and the timing of both cellular and
senescence in a mammal. Pituitary transplantation into dwarf mice does not
reverse the
lifespan effect, suggesting that the effect is not due to lowered prolactin
levels. In contrast,
homozygosity for the Ghrhrlit mutation, which like the Pit1dw mutation lowers
plasma growth
hormone levels, does lead to a significant increase in longevity. Male Snell
dwarf mice,
unlike calorically restricted mice, become obese and exhibit proportionately
high leptin
levels in old age, showing that their exceptional longevity is not simply due
to alterations in
adiposity per se. Further studies of the Pit1dw mutant, and the closely
related, long-lived
Prop-1df (Ames dwarf) mutant, should provide new insights into the hormonal
regulation of
senescence, longevity, and late life disease.

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