Another interesting November research article recently published deals with the shortening of telomeres as the missing link between aging and type 2 diabetes (AGING, 2010, Vol 2 no 10:650). As stated before telomere shortening, either because there is no telomerase activity or by some other mechanism, have been documented to be associated to diseases of aging. In the present study a group of scientist led by Michael Ristow used mice to establish a link between diabetes and telomere shortening. In their study, the group utilized mice that had their telomerase enzyme modified in such a way that it was inactivated. This resulted in telomere shortening and reduced replicative capacity of beta-cells (the pancreatic cells that produce insulin). The lack of insulin secretion and the increase of glucose intolerance can therefore be viewed as an aging-associated disorder and method of increasing telomerase activity could result in improvements in this disease.