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Obesity reversed in mice by destroying blood vessels that service fat cells

on the kind of organ or tissue they are supporting, the researchers say. Their idea is that if unique molecules can be located that define each different kind of blood vessel, then drugs can be targeted to those "addresses" to treat associated diseases.

Blood vessels that service adipose tissue that contains white fat cells is an example of this distinctive type of vasculature, they say. "White adipose tissue is unique because it resembles a tumor in that it can rapidly expand," says Kolonin. "For such rapid expansion, there must be a very active production of blood vessels to deliver oxygen, and in fact, every single fat cell is encased by capillaries."

Because of such a potential for biological activity, a vast network of blood vessels is needed to deliver oxygen to these cells - many more blood vessels than are needed to support other normal tissues, the researchers say. In fact, one pound of fat contains a mile of blood vessels, according to an estimate quoted by Harvard Medical School Professor Judah Folkman, M.D., the first researcher to promote the concept that adipose tissue mass may be controlled by angiogenesis (the process of new blood vessel formation from established ones).

Given their belief that blood vessels that feed adipose tissue are different from all other kinds of blood vessels, the M.D. Anderson researchers set out to find a protein marker or "zip code address" that would identify those particular vessels.

They did this by using an in vivo "phage display library" screening technique that the group developed. This method uses billions of viral particles that each displays a different peptide on its outer coat. In this study, researchers injected these genetically modified viruses into obese mice, hoping several peptides would bind onto protein receptors found only on the inside lining of adipose tissue blood vessels. The process was laborious, but after years of searching, they located a receptor that appears to
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9-May-2004


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