Thursday, 31 March 2011

Penn Researcher Links DNA Aging Clock to Diabetes

Penn Researcher Links DNA Aging Clock to Diabetes

Though some people stay energetic and wrinkle-free longer than others, we're all programmed to break down, deteriorate, and eventually, to die.

In our cells are tiny aging clocks made from pieces of DNA called telomeres. Rather than holding genes, the telomeres cap the ends of our DNA strands, preventing them from fatal fraying. Over the years, the telomeres shorten, like candle wicks, until they reach their ends.

Now, scientists are learning how Type 2 diabetes - the most common kind - is linked to the shortening of those telomeres.

On Tuesday at the University of Pennsylvania, medical researcher Mary Armanios spoke about her latest results in telomeres and diabetes - showing how the insulin-producing cells in the pancreas shut down when their telomeres erode to the end.

That understanding, she said, could lead to new approaches to treat or prevent the disease, which is growing more prevalent.

She presented her findings this month in the journal Public Library of Science One.

Armanios, who works at Johns Hopkins Kimmel Cancer Center, said she became interested in studying telomeres after meeting a college-age man with gray hair, lung problems, and bone-marrow failure, all caused by a genetic disease called dyskeratosis congenita. People with the disease have very short telomeres, so their aging clocks run out of time unusually fast.

The telomeres are often compared to caps on shoelaces because, when intact, they protect the parts of the genetic code at the ends of chromosomes.

Every time a cell divides, the telomeres get a little shorter. Once they're gone, a mechanism kicks in that causes the cells to die.

This might seem like something medical science would be scrambling to stop, but the cell death protects us from cancer by eventually stopping malignant cells from growing. So we can't just turn the whole thing off.

In her work, Armanios uses genetically engineered mice with unusually short telomeres, making these already short-lived creatures even quicker to gray and grow old. Besides all their other problems, these mice quickly develop high blood sugar, the hallmark of diabetes.

What seemed to be happening, she said, was that the animals' short telomeres were causing the premature shutdown of insulin-secreting cells. These cells aren't dead but put up a closed-for-business sign and stop doing anything. Armanios said perhaps their research would point to a way to wake them up.

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