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In a novel study, Dr. Preeti Kishore of Albert Einstein College of Medicine took 30 somewhat overweight but healthy volunteers and infused free fatty acids, a type of fat molecule, directly into their blood. She was mimicking what happens in the obese, when these fatty acids spill out from stored fat and continually flow through the body.
The results were startling: For five hours, the volunteers' bodies quit responding effectively to insulin. They also experienced a surge in a protein called PAI-1 (pronounced Pie-one) that sets off a chain reaction linked to heart disease-causing blood clots and diabetes. When Kishore took samples of the volunteers' fat tissue, she found the macrophages start producing more PAI-1 as they are bathed in the fatty acids.
The more pounds you put on, the bigger fat cells called adipocytes become until they release fatty acids and eventually die. The theory is that macrophages come in to clean up the dead cells but are hijacked to produce inflammation-causing chemicals -- signals that also spur further adipocyte dysfunction. Kishore's work suggests fat tissue primes macrophages to be switched on by a boost in fatty acids, starting the inflammation cycle.
"What's really exciting to us, is trying to understand these mechanisms can essentially help us to target therapies more effectively in the future," says Kishore, whose research was published last week in the journal Science Translational Medicine.
She points to Shoelson's study of salsalate -- which blocks a related protein found in macrophages and other immune cells -- as a first step.
"Four to five years ago, no one thought fat tissue matters for this stuff," adds Michigan's Lumeng, who studies the macrophage link. "There clearly are going to be anti-inflammatory therapies for diabetes coming out of the pipeline."
On the Net:
Salsalate diabetes study: http://tinyurl.com/yhop86s
Lauran Neergaard covers health and medical issues for The Associated Press in Washington.
Copyright 2010 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
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