Abstract
Background: The incidence of type 2 diabetes mellitus (T2DM) increased with advancing age. Older adults with T2DM were usually accompanied by gradual impairment of β-cell function and accumulation of senescent β-cells. However, the contribution of β cell senescence to diabetes has received little attention. Our previous study found that with increasing age of mice, knocking out the Cask gene in pancreatic islet β-cells leads to a gradual increase impairment in glucose profile and insulin secretion.
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