Leptin, a hormone that became famous in 1994 for its potential antiobesity effects, may also play a key role in the onset of puberty in mice, says a report in today's Science magazine.
Scientists have assumed that girls must achieve a threshold fat level in order to enter puberty. The new findings build on that hypothesis, says Farid F. Chehab, a researcher at the University of California, San Francisco (UCSF), and lead author of the study. Chehab suggests that leptin released by adipose tissue tells the body it has sufficient fat reserves to enter puberty and the reproductive years.
Chehab's work on prepubescent, healthy female mice was spurred by his observation that leptin could restore fertility in obese mice that had previously been sterile. After injecting 13 mice daily with leptin and administering a saline solution daily to 12 control mice, the UCSF researchers found that the leptin group entered its first estrous cycle sooner, had more advanced reproductive tracts, and reproduced up to 9 days earlier than the control mice. Similar results were reported late last year at the Society for Neuroscience meeting by endocrinologist Jeffrey Flier and colleagues at Beth Israel Hospital in Boston. (See ScienceNOW, 20 November.)
The results confirm that leptin "can initiate the cascade of events that leads to reproduction," Chehab says. The next question, he says, is understanding its relationship to the other factors in the reproductive cycle.
That question is controversial. While Chehab speculates that leptin acts directly on the brain, other researchers are looking elsewhere in the body. Scientists at Progenitor Inc., a Columbus, Ohio, biotechnology firm, for example, have found leptin receptors on the reproductive organs. "If the receptors are there, they should be doing something," says Joseph Cioffi, the company's director of genomics.
Leptin researchers are now exploring the possible routes by which the hormone influences reproductive maturity. In the meantime, says Robert Steiner, a leptin researcher at the University of Washington, the Chehab study offers "compelling testimony that leptin is certainly more than a simple satiety factor."