Age-related islet inflammation marks the proliferative decline of pancreatic beta-cells in zebrafish

Research output: Contribution to journalResearch articleContributedpeer-review



The pancreatic islet, a cellular community harboring the insulin-producing beta-cells, is 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 tnf alpha-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(hi) cells also exhibit premature upregulation of socs2, 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.


Original languageEnglish
Number of pages24
Publication statusPublished - 6 Apr 2018

External IDs

PubMed 29624168
Scopus 85046843174


Research priority areas of TU Dresden


  • Endoplasmic-reticulum stress, Large gene lists, In-vivo, Life, Replication, Activation, Apoptosis, Survival, Pathway, Glucose