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Growth Hormone's link to starvation may be
clue to increasing life span
Newswise — Researchers at UT
Southwestern Medical Center have determined
that starvation blocks the effects of growth
hormone via a mechanism that may have
implications in treating diabetes and
extending life span.
“It’s been well-established
that growth is blunted during starvation.
But our work shows that this is not just
from running out of energy. It’s much more
sophisticated than that,” said Dr. Steven
Kliewer, professor of molecular biology and
senior author of a study available online
and appearing in today’s issue of the
journal Cell Metabolism.
Using genetically altered
mice, the researchers found that during
fasting, the actions of growth hormone are
blocked by a fat-burning hormone called
FGF21.
“It’s something that we
hadn’t anticipated,” said Dr. Kliewer.
Growth hormone has many
functions in the growth and reproduction of
cells, such as controlling the length of
developing arm and leg bones in children.
Growth hormone has several
other functions, however, even in adults. It
promotes the breakdown of fats, stimulates
creation of protein and increases levels of
IGF-1 (insulin-like growth factor-1), a
hormone that promotes growth. Too much
growth hormone can cause insulin resistance,
resulting in diabetes, and lead to other
disorders.
In the current study, mice
that were genetically altered to produce
excess FGF21 grew to be much smaller than
ordinary mice, even though they ate more and
had more fat in proportion to their size.
Paradoxically, and to the researchers’
surprise, the altered, smaller mice produced
much greater amounts of growth hormone than
normal.
Why didn’t the altered mice
grow larger than normal in response? The
researchers found that FGF21 does not block
the production of growth hormone; rather, it
works to prevent growth hormone from
activating the genes it normally controls.
Interfering with the actions
of growth hormone has been shown to increase
life span in mice, Dr. Kliewer said.
“In addition, intermittent
fasting – which increases FGF21
concentrations – also extends life span in
mice. This raises the intriguing possibility
that FGF21 might be a longevity factor,” Dr.
Kliewer said.
“This is something that we’re
beginning to test in the lab,” he said. “But
our genetically engineered mice have all the
classic hallmarks of extended life span:
growth hormone resistance, low
concentrations of IGF-1, increased insulin
sensitivity and small size.”
FGF21 is already being tested
in human clinical trials for treatment of
obesity and diabetes in adults, but the new
findings linking FGF21 to interference with
growth hormone might indicate that caution
is needed before using it in children or
teens, Dr. Kliewer said.
Other UT Southwestern
researchers involved in the study were lead
author Dr. Takeshi Inagaki, instructor of
molecular biology; Dr. Vicky Lin,
postdoctoral research fellow in
pharmacology; and Dr. David Mangelsdorf,
chairman of pharmacology and a Howard Hughes
Medical Institute investigator. Dr. Moosa
Mohammadi from New York University School of
Medicine also participated in the study.
The work was supported by the
National Institutes of Health, the Welch
Foundation and the Howard Hughes Medical
Institute
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