New evidence has emerged from studies in mice that short telomeres, the endcaps of chromosomes, may predispose people to age-related diabetes.  Mary Armanios, from Johns Hopkins Medical Institutions (Maryland, USA), and colleagues observed that diabetes seems to occur more often in patients with dyskeratosis congenita, a rare, inherited disease caused by short telomeres. The team studied mice with short telomeres and their insulin-producing beta cells, finding that despite the presence of plentiful, healthy-looking beta cells, the animals had higher blood sugar levels and secreted half as much insulin as the controls. Specifically, in beta cells from mice with short telomeres, the researchers found disregulation of p16, a gene linked to aging and diabetes, with no such mistakes found in the controls.  In addition, many of the gene pathways essential for insulin secretion in beta cells, including pathways that control calcium signaling, were altered in beta cells from mice with short telomeres.