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Learn MoreImmature -cells are present in adult islets. However, their contribution to insulin release is not fully understood. Here we show that specific loss of immature -cells induces failure throughout the -cell complement. Functional mapping of the -cell population in rodent and human loss-of-immaturity islets revealed defects in metabolism, ionic fluxes and insulin secretion. At the transcriptomic level, loss of immature -cells led to dysregulation of gene pathways involved in glucose and carbohydrate-derivative metabolic processes. Using a chemogenetic disruption strategy, immature -cells were found to depend on the islet signaling network for their phenotype. During metabolic stress, islet function could be restored by redressing the balance between immature and mature -cells. We thus unveil immature -cells as a critical component in islet operation. Preserving immature -cells might be important for islet engineering efforts and more broadly the treatment of type 1 and type 2 diabetes. SOURCE: ildem akermanAkerman Lab University of Birmingham
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