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Genetic Recording of Pancreatic Beta Cell Proliferation

ABSTRACT: Pancreatic beta cell generation and proliferation primarily rely on self-renewal of pre-existing beta cells, making precise quantification of beta cell proliferation essential for understanding pancreatic homeostasis and pathogenesis. However, technical limitations have previously restricted the ability to trace beta cell proliferation in vivo over extended periods. Here, we developed beta cell-ProTracer, a genetic system utilizes dual recombinase technology to enable continuous and cell type-specific recording of beta cell proliferation in mice. The beta cell-ProTracer system allows for the quantification of the proliferation rate of adult pancreatic beta cells during homeostasis and in response to injury or drug treatment. Clonal analysis of the proliferated beta cell population reveals a uniform proliferative capacity among these cells. Our findings enhance the understanding of beta cell proliferation dynamics in pancreatic homeostasis, repair, and regeneration.

ORGANISM(S): Mus musculus

PROVIDER: GSE313841 | GEO | 2026/01/22

REPOSITORIES: GEO

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Project description:Obesity is associated with an increase in β-cell mass in response to the rising demand for insulin. β-cell plasticity is essential to maintaining glucose homeostasis, however, the cellular and molecular mechanisms by which β-cell mass is regulated remain poorly understood. Recently, we described the existence of a crosstalk between the peripancreatic adipose tissue and β-cells as a novel mechanism that participates in the regulation of β-cell plasticity. Here, we identify the secreted frizzled-related protein (Sfrp) 5 as down-regulated in the pancreatic islets of obese rats as well as in the pancreatic islets of human obese patients. Our results demonstrate that the silencing of Sfrp5 induces an increase in β-cell proliferation, which we correlate with the activation of Wnt signaling and of the MAPK and PI3 kinase pathways. Together, these findings expand our understanding of the mechanisms underlying β-cell proliferation under conditions of obesity. Furthermore, this study opens new insights into the specific targeting of Sfrp5 as a novel therapeutic strategy for balancing β-cell mass. Adult male Wistar rats (Charles River Laboratories, Wilmington, MA), 7 wk old (weighing 225–250 g), were caged individually in a 12-h light, 12-h dark cycle in a temperature- and humidity-controlled environment. Animals were divided into two dietary sets for 10 days. One group was fed with standard chow diet (supplying 8% of calories as fat; type AO4 from Panlab, Barcelona, Spain). The second group was fed with a cafeteria diet (66% of calories as fat), as previously described (Endocrinology 2012;153:177-87). Pancreatic islets were isolated through collagenase perfusion of the pancreas, Histopaque gradient and hand-picking under microscopic guidance. Ten micrograms of total RNA from islets were converted into cRNA, biotinylated, fragmented, and hybridized to GeneChip Rat Genome 230 2.0 (Affymetrix, Santa Clara, CA). Ten microarrays were hybridized, five with independent samples coming from rats fed with standard chow (lean group) and five with independent samples coming from rats fed with the cafeteria diet (obese group).

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Genetic Recording of Pancreatic Beta Cell Proliferation

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