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5 December 2013 11:26 am ,
Vol. 342 ,
At age 30, Dutch biologist Freek Vonk has built up a respectable career as a snake scientist. But in his home country,...
Since arriving on the island of Guam in the 1940s, the brown tree snake ( Boiga irregularis ) has extirpated native...
An animal rights group known as the Nonhuman Rights Project filed lawsuits in three New York courts this week in an...
Researchers have been hot on the trail of the elusive Denisovans, a type of ancient human known only by their DNA and...
Thousands of scientists in the Russian Academy of Sciences (RAS) are about to lose their jobs as a result of the...
Dyslexia, a learning disability that hinders reading, hasn't been associated with deficits in vision, hearing, or...
Exotic, elusive, and dangerous, snakes have fascinated humankind for millennia. They can be hard to find, yet their...
Researchers have sequenced and analyzed the first two snake genomes, which represent two evolutionary extremes. The...
- 5 December 2013 11:26 am , Vol. 342 , #6163
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Plumping Your Way to Disease
11 May 2006 (All day)
As if fat didn't give us enough trouble, a new study provides further evidence that cellulite can release disease-causing compounds. Overweight individuals generate increased amounts of a protein called monocyte chemoattractant protein-1 (MCP-1) from their fat tissue, and mice producing high levels of this protein develop insulin resistance, a precursor to diabetes.
Over the past few years, researchers have realized that fat tissue is more than just extra baggage. It excretes dozens of substances called adipokines that act as hormones and inflammatory agents (ScienceNOW, 2 April 2004). MCP-1 is one of these substances, and it tends to be elevated in the blood of people who are overweight. Numerous studies have shown that excess fat leads to insulin resistance. But evidence directly linking MCP-1 to diabetes was lacking.
So researchers from Kobe University in Japan genetically engineered mice that produce very high levels of MCP-1. They found that these mice rapidly develop insulin resistance and accumulate fat in the liver, which may lead to high cholesterol levels. The team also engineered mice that do not make the MCP-1 protein at all; these mice experience less insulin resistance and liver fat than normal mice. Finally, blocking MCP-1 activity in both normal mice and overweight mice seems to slow the development of insulin resistance, lowering the risk for diabetes, the team reports online today in the Journal of Clinical Investigation.
Experts believe that MCP-1 isn’t the only signaling molecule responsible for insulin resistance. Researchers are trying to identify these other factors and how they interrelate, says Anthony Ferrante, a diabetes specialist at the Columbia University Medical Center in New York City. Still, many are hoping that the new findings will lead to better medications to treat diabetes. "It certainly is an interesting possibility," says Philip Kern from the University of Arkansas for Medical Sciences in Little Rock. But, he says, drug development may be tricky: MCP-1 plays an important role in fighting injuries, infections, and cancer, so a drug that blocks MCP-1's actions might lead to unwanted side-effects.