The pancreatic islet， a cellular community harboring the insulin-producing beta-cells， is known to undergo age-related alterations. However， only a handful of signals associated with aging have been identified. By comparing beta-cells from younger and older zebrafish， here we show that the aging islets exhibit signs of chronic inflammation. These include recruitment of -expressing macrophages and the activation of NF-kB signaling in beta-cells. Using a transgenic reporter， we show that NF-kB activity is undetectable in juvenile beta-cells， whereas cells from older fish exhibit heterogeneous NF-kB activity. We link this heterogeneity to differences in gene expression and proliferation. Beta-cells with high NF-kB signaling proliferate significantly less compared to their neighbors with low activity. The NF-kB signaling cells also exhibit premature upregulation of ， an age-related gene that inhibits beta-cell proliferation. Together， our results show that NF-kB activity marks the asynchronous decline in beta-cell proliferation with advancing age.