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Aims/Introduction  Impaired growth and premature death of β‐cells are implicated in the progression of islet pathology in type 2 diabetes. It remains unclear, however, how aging affects islet cells, or whether the islet change in diabetes is an augmented process of aging. We studied age‐related changes of the islet structure in  J apanese non‐diabetic subjects and explored the underlying mechanism of the changes.    Materials and Methods  A total of 115 non‐diabetic autopsy cases were subjected to morphometric analysis for volume densities of islets, β‐ and non‐β‐cells, as well as their masses. Proliferation activity identified by  K i67, and expressions of pancreatic and duodenal homeobox ( PDX )‐1, cell cycle inhibitor  P 16, and oxidative stress marker γ H 2 AX  were also examined.    Results  There was a gradual and marginal decline of volume densities of islets, β‐ and non‐β‐cells with aging, while masses of these components were increased during maturation and slowly decreased after the 40s. Islet density was high in the young, but reduced after maturation. There was only a minimal influence of increased body mass index ( BMI ) on the increase in β‐cell mass, but not on the other variables.  K i67 positivity and  PDX ‐1 expressions were high in the young, but low after maturation, whereas expressions of  P 16 and γ H 2 AX  were elevated in the aged.    Conclusions  Age‐associated decline of β‐cell mass is marginal after maturation, and the reduction of β‐cell mass could be a specific process in diabetes. The impact of  BMI  on the islet structure is limited in  J apanese with normal glucose tolerance.

Age‐associated changes of islet endocrine cells and the effects of body mass index in J apanese