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Neonatal infections impair islet maturation and long-term glucose homeostasis by disturbing the pancreatic macrophage population.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Cell Biology.
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Abstract [en]

The development of the pancreatic islet occurs late during pregnancy and continues in the neonate with β cell development of functional maturity. Here we show that pancreatic macrophages are present in highest densities in the neonate. In addition, we found that transient neonatal infections reduced the numbers of pancreatic macrophages and resulted in development of impaired glucose tolerance that persisted into adolescence when the infection was cleared and macrophage levels were restored (three- and six-week-old mice). Reduced islet insulin content and β cell proliferation, together with decreased proportion of MafA+ β cells, were observed in six-week-old mice subjected to neonatal infections. Transient neonatal depletion of macrophages recapitulated the effects of neonatal infections: longstanding impairment of glucose homeostasis and reduced β cell proliferation (six-week-olds), indicating a role for macrophages in postnatal islet maturation. Our findings uncover a novel function for macrophages in securing appropriate postnatal islet development. Immune challenges occurring at this time distracted the pancreatic macrophage population and hindered islet maturation, thereby resulting in longstanding impairment of glucose homeostasis. 

Keywords [en]
Macrophages, postnatal pancreas development, β cell maturation, infections, glucose homeostasis
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Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-395529OAI: oai:DiVA.org:uu-395529DiVA, id: diva2:1362482
Available from: 2019-10-20 Created: 2019-10-20 Last updated: 2019-10-27
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