Shortened β-cell lifespan leads to β-cell deficit in a rodent model of type 2 diabetes

Shortened beta-cell lifespan leads to beta-cell deficit in a rodent model of type 2 diabetes. Am J Physiol Endocrinol Metab 300: E933-E938, 2011. First published February 22, 2011; doi: 10.1152/ajpendo.00504.2010.-Since the fundamental defect in both type 1 and type 2 diabetes is beta-cell failure, there is increasing interest in the capacity, if any, for beta-cell regeneration. Insights into typical beta-cell age and lifespan during normal development and how these are influenced in diabetes is desirable to realistically establish the prospects for beta-cell regeneration as means to reverse the deficit in beta-cell mass in diabetes. We assessed the mean beta-cell age and lifespan by the classical McKendrick-von Foester equation that describes the age-based heterogeneity of beta-cells in terms of the time-varying beta-cell formation and loss estimated by a beta-cell turnover model. This modeling approach was applied to evaluate beta-cell lifespan in a rodent model of type 2 diabetes in comparison with nondiabetic controls. When rats were 10 mo old, mean beta-cell lifespan was 1 mo vs. 6 mo in rats with type 2 diabetes vs. controls. A shortened beta-cell lifespan in a rat model of type 2 diabetes results in a decrease in mean beta-cell age and thus contributes to decreased beta-cell mass.