LITTLE ROCK, Arkansas - Scientists in Arkansas have identified a synthetic estrogen-like compound that reverses bone loss in mice without affecting the reproductive system, as does conventional hormone replacement therapy. The finding, reported in the Oct. 25 edition of Science, could lead to new therapies to prevent osteoporosis for millions of women and men, and enable safer alternatives to existing hormone treatments, shown earlier this year to pose more serious risks than previously thought.

"We are developing a new class of pharmaceutical agents with the potential for bone-building, sex-neutral hormone replacement therapy," said lead investigator Stavros C. Manolagas, MD, PhD, an endocrinologist with the Central Arkansas Veterans Health Care System and the University of Arkansas for Medical Sciences. He also directs the Osteoporosis and Metabolic Bone Diseases Center in Little Rock, a research laboratory established jointly by VA and UAMS.

Manolagas' team reported last year in the journal Cell that sex hormones exert their bone-protecting and reproductive effects through separate cellular mechanisms--one fast-acting and non-sex-specific, the other long-term and sex-specific. The researchers also identified a synthetic estrogen-like hormone--"estren"--to work in one pathway but not the other. This earlier study, conducted with mouse bone cells, suggested the possibility of gender-neutral hormone replacements that could produce benefits to the bone without reproductive side effects.

The new study is the first time scientists have demonstrated in animals how synthetic hormones can build bone without affecting reproductive organs.

Manolagas and colleagues tested the effects of estren, compared to conventional estrogen and testosterone, in male and female mice. Some of the mice had their ovaries or testis removed, to halt the production of their natural sex hormones. These mice showed a 6-percent loss in bone density, a 23-perc
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Contact: Derenda Summerlin
derenda.summerlin@med.va.gov
501-257-3287
VA Research Communications Service
24-Oct-2002

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