Title: Spatial resolution of extraendocrine Slit2/3 in compensatory islet expansion
Abstract: Pancreatic islets are endocrine cell clusters that regulate blood glucose homeostasis through the secretion of hormones such as insulin, glucagon, and somatostatin. While islet structure is stable in homeostatic conditions, islets expand during obesity and prediabetes to compensate for increasing metabolic demands. In mice, islet cells are organized as a core of beta cells surrounded by a mantle of alpha and delta cells, with evidence suggesting that this arrangement is important for optimal islet function of coordinated hormone release. Formation of islet architecture requires expression of Roundabout receptors 1 and 2 (Robo1/2) in endocrine cells and of Slits 2 and 3 (Slit2/3) from islet-extrinsic sources, with the top candidate being pancreatic mesenchyme. To spatially identify sources of Slit2/3 expression at the single-cell resolution, we performed simultaneous fluorescent in situ hybridization and protein detection, followed by confocal imaging and quantitative analysis using QuPath. We provide resolution of Slit2/3 expression in wild-type and Ob/Ob diabetic mouse models and specifically illustrate a decrease in Robo2 expression and an increase in Slit3 expression in diabetes. These results demonstrate that Slit2/3 and Robo1 may have important roles in maintaining islet function during islet expansion.
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