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. Author manuscript; available in PMC: 2020 Nov 6.
Published in final edited form as: Diabetologia. 2020 Sep 7;63(10):2030–2039. doi: 10.1007/s00125-020-05210-8

Fig. 1.

Fig. 1

Schematic showing normal pancreatic morphology (a) with close proximity between pancreatic ducts, acini and islets, the latter comprising beta cells, alpha cells, delta cells and PP cells with resident macrophages (cell types shown in key). Capillaries and autonomic nerve fibres supply all pancreatic compartments. Generalised alterations in pancreatic morphology that occur with pancreatogenic diabetes (b), i.e. ductal plugging (shown in pink within the duct lumen)/dilation, fibro-fatty replacement of acinar tissue and lymphocyte infiltration, with macrophages in the exocrine pancreas but not within the islet, and islet remodelling (modest loss of beta cells and increase in alpha cells). Micrographs showing H&E-stained pancreas sections from a control individual without pancreatic disease (c) an individual with chronic pancreatitis (d) and a person with cystic fibrosis (e). Islets are demarcated with dotted black lines, a normal duct is shown with an arrow in (c), fibrosis is shown surrounding degenerating acini (the latter denoted by arrowheads) in (d) and extensive fatty replacement of exocrine pancreas is shown in (e). Strikingly, despite the severe disruption to the exocrine pancreas in (d) and (e), islets remain readily visible. Scale bar, 100 μm.