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- W3100915805 abstract "Pancreatic beta-cell death occurs in diabetes and contributes to hyperglycemia. By sampling the local tissue environment, macrophages act as critical gatekeepers of tissue homeostasis in health and disease. Here, we show that, following beta-cell death, islet macrophages acquire a state of heightened IGF-1 secretion, decreased proinflammatory cytokine expression, and transcriptome changes indicative of altered cellular metabolism. This was consistently observed across three rodent models of type 2 diabetes and islet macrophages were identified as the exclusive local source of IGF-1. Neither high blood glucose nor high fat diet altered the activation state of these immune cells. Depletion of macrophages and IGF-1 neutralization both worsened streptozotocin-induced glucose tolerance, while adoptive transfer of bone-marrow-derived macrophages reduced glycemia and enhanced plasma insulin levels. Our data suggest increasing the number or functionality of islet macrophages may be an approach to preserve functional beta-cell mass in individuals with diabetes." @default.
- W3100915805 created "2020-11-23" @default.
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- W3100915805 date "2018-11-27" @default.
- W3100915805 modified "2023-09-22" @default.
- W3100915805 title "Islet macrophages are the primary islet source of IGF-1 and improve glucose homeostasis following pancreatic beta-cell death." @default.
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