Pancreatic function and diabetes
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This study identifies a gene that could potentially be targeted in human pancreatic duct cells to replenish β cell mass for diabetes therapy by using a genome-wide clustered regularly interspaced short palindromic repeats screen.
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Replenishment of pancreatic β cells is key to a cure for diabetes. β cell regeneration is achieved predominantly by self-replication, especially in rodents, but it was also shown that pancreatic duct cells can transdifferentiate into β cells. How pancreatic duct cells are transdifferentiated and whether we can manipulate transdifferentiation to replenish β cell mass are not well understood. Using a genome-wide clustered regularly interspaced short palindromic repeats (CRISPR) screen, we found that the loss of function of aldehyde dehydrogenase family 3 member B2 ( ALDH3B2 ) was sufficient to transdifferentiate cell line–based and human pancreatic duct cells into functional β-like cells. The transdifferentiated cells had substantially increased the expression of β cell marker genes, secreted insulin in response to glucose, and lowered blood glucose to near normal for 6 weeks after transplantation into streptozotocin-induced diabetic mice under the kidney capsule. Our study identifies a gene that could potentially be targeted in human pancreatic duct cells to replenish β cell mass for diabetes therapy.
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@article{Li2026Loss,
title = {Loss of function of ALDH3B2 transdifferentiates human pancreatic duct cells into β-like cells},
author = {Jian Li and Kevin Bode and Yu‐Chi Lee and Noelle Morrow and Andy Ma and Mulin He and Siying Wei and Jessica da Silva Pereira and Taylor Stewart and Alexander Lee-Papastavros and Jennifer Hollister‐Lock and Brooke A. Sullivan and Hui Pan and Jonathan M. Dreyfuss and Susan Bonner‐Weir and Yi Peng},
journal = {Science Translational Medicine},
year = {2026},
doi = {10.1126/scitranslmed.ady2234},
url = {https://doi.org/10.1126/scitranslmed.ady2234}
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