New evidence has emerged from studies in mice that short telomeres or "caps" at the ends of chromosomes may predispose people to age-related diabetes, according to Johns Hopkins scientists and colleagues. Telomeres are repetitive sequences of DNA that protect the ends of chromosomes, and they normally shorten with age, much like the caps that protect the ends of shoelaces. As telomeres shorten, cells lose the ability to divide normally and eventually die. Telomere shortening has been linked to cancer, lung disease, and other age-related illnesses. Diabetes, also a disease of aging, affects as many as one in four adults over the age of 60. The Johns Hopkins research, described online on March 10, 2011, in PLoS ONE, arose from Dr. Mary Armanios' observation that diabetes seems to occur more often in patients with dyskeratosis congenita, a rare, inherited disease caused by short telomeres. Patients with dyskeratosis congenita often have premature hair graying and are prone to develop early organ failure. "Dyskeratosis congenita is a disease that essentially makes people age prematurely. We knew that the incidence of diabetes increases with age, so we thought there may be a link between telomeres and diabetes," said Dr. Armanios, assistant professor of oncology at the Johns Hopkins Kimmel Cancer Center. Dr. Armanios studied mice with short telomeres and their insulin-producing beta cells. Human diabetics lack sufficient insulin production and have cells resistant to its efficient use, causing disruption to the regulation of sugar levels in the blood. Dr. Armanios found that despite the presence of plentiful, healthy-looking beta cells in the mice, they had higher blood sugar levels and secreted half as much insulin as the controls.
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