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Loss of Estrogen Receptors
Linked to Osteoporosis
by
Patricia Reaney
Reuters Health, Wednesday, July 23, 2003
LONDON (Reuters) - Older women may be more prone
to suffer from osteoporosis because they do not have enough receptors,
or chemical doorways, for the female hormone estrogen, scientists said
on Wednesday.
Osteoporosis, or brittle bone disease, affects
about one in three women and is more common after the menopause when
the body makes less estrogen.
Normally when a bone is subjected to repeated
mechanical stress, new bone cells compensate for the load. But Professor
Lance Lanyon and researchers at The Royal Veterinary College in London
have discovered that in transgenic mice lacking an estrogen receptor
called ER-alpha, this does not happen.
"It is the first time ER-alpha has been
implicated in bones' normal adaptive response to mechanical loading," Lanyon
said in an interview.
"The estrogen receptor is involved in the
response to mechanical loading which is responsible for establishing
and maintaining bone mass. We think that is the critical link why when
you take away the reproductive hormone, you lose bone," he added.
Hormone replacement therapy (HRT), which replenishes
the hormone loss after menopause, is prescribed to prevent osteoporosis
but it can increase the risk of heart disease, strokes and some cancers.
"The rationale for why hormone replacement
therapy prevents osteoporosis is that if it has estrogen in it, it
maintains estrogen receptor numbers," said Lanyon.
But the disadvantage is that high estrogen receptors
in breast or uterine tissue could increase the likelihood of developing
cancer in those areas.
Lanyon believes his findings, which are reported
in the science journal Nature, could lead to the development of new
drugs that could enhance the performance of the receptor for bone density
without increasing cancer risk.
"The future trick would be to get an organ
or tissue-specific enhancement of estrogen receptor activity just for
the bones and not for the other tissues," he added.
Lanyon said the research points to a specific
therapeutic strategy to prevent osteoporosis and answers the long-standing
puzzle about why removing a reproductive hormone results in bone loss.
SOURCE: Nature, 2003.
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