X-Message-Number: 27652
Date: Sat, 25 Feb 2006 11:03:52 -0800 (PST)
From: Doug Skrecky <>
Subject: growth hormone exacerbates renal disease in rats

[The induction of higher levels of insulin, may have down-regulated
macroautophagy, which then accelerated the decline in renal function in
obese Zucker rats. A threshold level of macroautophagy has been found to
be an obligatory process for maintaining longterm tissue homeostatis.]

Exp Biol Med (Maywood). 2006 Jan;231(1):76-83.
Effect of long-term somatotropin treatment on body composition
and life span in aging obese Zucker rats.
The objective of this work was to test the hypothesis that a
somatotropin (STH)-induced reduction in body fat would prolong
the life span of the obese Zucker rat. Two experiments were
conducted. In the first experiment, male and female, lean and
obese Zucker rats were treated with STH (0 or 2 mg/d bovine STH)
for 4 weeks, beginning at 7 months of age. Across phenotypes, STH
treatment increased the growth rate by 159%, muscle weights by 14%,
and circulating insulin-like growth factor (IGF)-1 by 23%, and
decreased carcass fat by 21% (P < 0.05). The second experiment was
a longevity trial to determine whether these changes in body
composition would increase the life span of the obese rat. Beginning
at 7 months of age, individually housed, male and female, lean and
obese rats were assigned to daily STH treatments (0 or 2 mg/d).
Rats were monitored daily, and sick or moribund rats were
euthanized and necropsied to determine existing pathologies. The
average life span of the lean rats was 661 days and was unaffected
by STH treatment (639 days, NS) or gender. Average life span of
the vehicle-injected obese rats (435 days) was less than that of
the lean group (P < 0.001). STH treatment of the obese rats
resulted in a further reduction of life span (349 days, P < 0.02).
The predominant pathology observed across the treatment groups was
renal disease, characterized by progressive glomerulonephropathy.
Thus, although exogenous STH was able to reduce carcass lipid and
to increase lean tissue mass in obese rats, there was no
improvement in longevity. In contrast to the hypothesis, STH
actually reduced the life span of the obese rat. It is likely
that STH treatment accelerated the development of progressive
glomerulonephropathy in the obese rat.

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