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Updated: Nov 17, 2025
A High-content In Vitro Pancreatic Islet β-cell Replication Discovery Platform
Published on: July 16, 2016
Pancreatic β cell regeneration induced by clinical and preclinical agents
Kang-Li Wang1, Ming Tao2, Tian-Jiao Wei1
1Department of Endocrinology and Metabolism, Peking University Third Hospital, Beijing 100191, China.
Abstract:
Diabetes, one of the most common chronic diseases in the modern world, has pancreatic β cell deficiency as a major part of its pathophysiological mechanism. Pancreatic regeneration is a potential therapeutic strategy for the recovery of β cell loss. However, endocrine islets have limited regenerative capacity, especially in adult humans. Almost all hypoglycemic drugs can protect β cells by inhibiting β cell apoptosis and dedifferentiation via correction of hyperglycemia and amelioration of the consequent inflammation and oxidative stress. Several agents, including glucagon-like peptide-1 and γ-aminobutyric acid, have been shown to promote β cell proliferation, which is considered the main source of the regenerated β cells in adult rodents, but with less clarity in humans. Pancreatic progenitor cells might exist and be activated under particular circumstances. Artemisinins and γ-aminobutyric acid can induce α-to-β cell conversion, although some disputes exist. Intestinal endocrine progenitors can transdeterminate into insulin-producing cells in the gut after FoxO1 deletion, and pharmacological research into FoxO1 inhibition is ongoing. Other cells, including pancreatic acinar cells, can transdifferentiate into β cells, and clinical and preclinical strategies are currently underway. In this review, we summarize the clinical and preclinical agents used in different approaches for β cell regeneration and make some suggestions regarding future perspectives for clinical application.
Insights
Regenerating pancreatic beta cells is key for treating diabetes. Research explores various agents and cell sources to restore beta cell function, offering new hope for diabetes therapy.
Area of Science:
- Endocrinology and Metabolism
- Regenerative Medicine
- Diabetes Pathophysiology
Background:
- Diabetes mellitus is characterized by pancreatic beta cell deficiency.
- Limited regenerative capacity of pancreatic islets, especially in adults, hinders recovery.
- Current hypoglycemic drugs offer some beta cell protection but regeneration remains a challenge.
Purpose of the Study:
- To review clinical and preclinical agents for pancreatic beta cell regeneration.
- To explore different therapeutic strategies for restoring beta cell mass and function.
- To provide future perspectives for clinical applications in beta cell regeneration.
Main Methods:
- Review of existing literature on agents promoting beta cell proliferation and survival.
- Analysis of studies investigating cell conversion (alpha-to-beta, intestinal progenitors, acinar cells) into insulin-producing cells.
- Examination of strategies targeting pancreatic progenitor cells and their activation.
Main Results:
- Several agents, including glucagon-like peptide-1 and gamma-aminobutyric acid, promote beta cell proliferation.
- Evidence suggests alpha-to-beta cell conversion and transdifferentiation of other cell types into beta cells.
- FoxO1 inhibition and activation of pancreatic progenitor cells are emerging strategies.
Conclusions:
- Beta cell regeneration holds significant therapeutic potential for diabetes.
- Multiple avenues, including cell proliferation, conversion, and transdifferentiation, are being explored.
- Further research is needed to translate these preclinical findings into effective clinical applications.
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