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Scientists Spot Fat Cell 'On' Switch

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  • TUESDAY, June 22 (HealthDayNews) -- With just one key signal, stem cells in mice develop into fat cells, says a Johns Hopkins Medical Institutions study.

    Researchers found that the addition of a single protein, called BMP4, induced mouse stem cells to turn into fat cells. They suspect that a similar chemical switch works the same way in human stem cells.

    The findings offer a deeper understanding of how humans store excess food energy in the form of fat, and could pave the way for drugs that short-circuit that process, the researchers said.

    The mouse stem cells used in this study have the ability to become muscle, bone, cartilage or fat. More than a decade ago, scientists identified the signals that direct the stem cells to turn into muscle or bone. But until now, the signal that switched on fat cells remained a mystery.

    "Apart from the muscle- and bone-inducing signals, not much is known about the initial switch from stem cell to labeled 'pre-fat' cell," researcher Daniel Lane, a professor of biological chemistry, said in a prepared statement.

    "BMP4 is the first proven fat-cell producing signal for these stem cells," Lane said.

    When he and his colleagues implanted BMP4-treated stem cells under the skin of mice, the stem cells developed into fat tissue that was indistinguishable from the animals' natural fat tissue.

    "Once we know the detailed mechanism of BMP4-signalling in fat cells, we can create drugs that interfere with the generation of stem cells, and we may be able to create drugs that interfere with the generation of fat cells in both the cell culture and live animal model systems," researcher Dr. Qi-Qun Tang, assistant professor of pediatrics and biological chemistry, said in a prepared statement.

    The study appears in the June 21 issue of the journal Proceedings of the National Academy of Sciences.

    More information

    The National Institutes of Health has more about weight control.

    (SOURCE: Johns Hopkins Medical Institutions news release, June 21, 2004)

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