Research Article: Type 2 Diabetes and the Aging Pancreatic Beta Cell

Date Published: June 28, 2011

Publisher: Impact Journals LLC

Author(s): Uma Gunasekaran, Maureen Gannon.



The incidence of and susceptibility to Type 2 diabetes increases with age, but the underlying mechanism(s) within beta cells that contribute to this increased susceptibility have not been fully elucidated. Here we review how aging affects the proliferative and regenerative capacity of beta cells and how this impacts beta cell mass. In addition we review changes that occur in beta cell function with age. Although we focus on the different rodent models that have provided insight into the characteristics of the aging beta cell, the limited knowledge from non-rodent models is also reviewed. Further studies are needed in order to identify potential beta cell targets for preventing or slowing the progression of diabetes that occurs with age.

Partial Text

The incidence and prevalence of Type 2 diabetes increases with age [1, 2]. It now affects approximately 18-30% of the elderly population in the United States [3, 4]. The underlying mechanism(s) behind why diabetes is increasing in the elderly is still not clearly understood. It has been hypothesized that insulin resistance increases with age due to increased adiposity, decreased lean muscle mass, changes in dietary habits, and reduced physical activity [5]. However, it has been shown that these factors alone do not account for age-related glucose intolerance [1]. Many human studies, some of which are summarized below, have tried to clarify the mechanism by which age-related glucose tolerance develops but have had contradictory results.

An increased incidence of diabetes is observed with age, and there are many possibly reasons for this. One of these is that the beta cell has reduced proliferative capacity and in diabetic individuals this is further confounded by higher rates of beta cell apoptosis. The currently known underlying mechanisms behind the reduction in beta cell proliferation observed with age include reduced expression of cell cycle activators, increased expression of cell cycle inhibitors, reduced pdx1 expression, and increased amylin aggregation. Studying aging in the non-diabetic rodent and human models is currently a developing field; therefore very few broad conclusions can be drawn. Further study in these areas is important as they could indicate targets for preventing or slowing the progression of diabetes with age.





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