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The Role of Pancreatic Beta-Cells in Obesity and Type 2...
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The Role of Pancreatic Beta-Cells in Obesity and Type 2 Diabetes

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 July 2026 | Viewed by 1988

Special Issue Editors

Dr. Mayur Doke

E-Mail Website
Guest Editor
Diabetes Research Institute, University of Miami Miller School of Medicine (UM-MSoM), Miami, FL, USA
Interests: spatial transcriptomics; single-cell RNA-seq; beta-cell regeneration; type 1 diabetes; pancreatic biology; ductal-to-beta cell differentiation
Prof. Dr. Juan Domínguez-Bendala

E-Mail Website
Guest Editor
Diabetes Research Institute, University of Miami Miller School of Medicine (UM-MSoM), Miami, FL, USA
Interests: pancreatic regeneration; stem cell therapy; beta-cell differentiation; type 2 diabetes; islet biology
Dr. Oscar Alcazar

E-Mail Website
Guest Editor
Diabetes Research Institute, University of Miami Miller School of Medicine (UM-MSoM), Miami, FL, USA
Interests: type 1 diabetes; pancreatic islet transplantation; islet biology

Special Issue Information

Dear Colleagues,

The rising prevalence of Type 2 Diabetes (T2D) and obesity worldwide underscores the urgent need for deeper understanding of pancreatic beta-cell biology. This Special Issue aims to explore the molecular, cellular, and metabolic mechanisms by which beta-cells adapt—or fail to adapt—to increased insulin demand in the context of obesity and T2D. We welcome submissions focusing on beta-cell proliferation, dedifferentiation, apoptosis, stress responses, and the role of incretin-based therapies such as GLP-1 receptor agonists in beta-cell preservation and regeneration. Studies leveraging cutting-edge technologies, including single-cell omics, lineage tracing, and spatial transcriptomics, are particularly encouraged. This Special Issue provides a platform for researchers to share discoveries that could shape future therapeutic strategies in diabetes care.

Dr. Mayur Doke
Prof. Dr. Juan Domínguez-Bendala
Dr. Oscar Alcazar
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • pancreatic beta-cells
  • GLP-1
  • obesity
  • type 2 diabetes
  • islet biology
  • beta-cell regeneration
  • insulin resistance
  • incretin therapies
  • single-cell transcriptomics
  • metabolic stress

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Published Papers (3 papers)

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21 pages, 4135 KB  
Article
The Role of Pancreatic Preproglucagon in Regulating Local Inflammation in Mice
by Ellen M. Zalucha, Chelsea R. Hutch, Maigen Bethea, Tyler M. Cook, Aayush Unadkat, Kristen L. Wells, Ki-Suk Kim, Basma Maerz, Michael Lehrke, Kanakadurga Singer and Darleen A. Sandoval
Cells 2026, 15(5), 482; https://doi.org/10.3390/cells15050482 - 6 Mar 2026
Viewed by 639
Abstract
Data suggest that both pancreatic and intestinally produced glucagon-like peptide-1 (GLP-1) increases in response to inflammation. Here, we set out to determine the tissue-specific function of increased GLP-1 during inflammatory stimuli. Using our innovative mouse model of tissue-specific Gcg (the gene that encodes [...] Read more.
Data suggest that both pancreatic and intestinally produced glucagon-like peptide-1 (GLP-1) increases in response to inflammation. Here, we set out to determine the tissue-specific function of increased GLP-1 during inflammatory stimuli. Using our innovative mouse model of tissue-specific Gcg (the gene that encodes GLP-1) expression, we explored the function of GLP-1 under severe inflammatory conditions induced by lipopolysaccharide (LPS) administration in lean and obese mice. High-fat diet (HFD) increased the LPS-induced suppression of feeding and increased the plasma levels of pro-inflammatory cytokines and GLP-1. Both pancreatic and intestinal Gcg expression contribute to LPS-induced increases in GLP-1, but Gcg was not necessary for the glucoregulatory or suppressed feeding responses to LPS. While Gcg was not necessary for systemic cytokine increases with LPS in either chow- or HFD-fed mice, whole-body Gcg-null animals had increased macrophage accumulation and an increased expression of genes reflecting pro-inflammatory signaling in the pancreas. We then performed flow cytometry on the pancreas from mice expressing a fluorescent marker on the GLP-1 receptor (GLP-1R). In response to LPS, we found that pancreatic CD64+/CD11b+ macrophages expressed the GLP-1R. We conclude that under severe inflammatory conditions, pancreatic production of GLP-1 functions in an immunological rather than a metabolic role to directly regulate local macrophage accumulation. Full article
(This article belongs to the Special Issue The Role of Pancreatic Beta-Cells in Obesity and Type 2 Diabetes)
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Review

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14 pages, 1037 KB  
Review
Mitochondria as Epigenetic Regulators of β-Cell Identity and Plasticity: A Metabolo-Epigenetic Perspective
by YongKyung Kim
Cells 2026, 15(7), 595; https://doi.org/10.3390/cells15070595 - 27 Mar 2026
Viewed by 214
Abstract
The progressive decline in functional β-cell mass in Type 2 Diabetes (T2D) is increasingly recognized not as a simple apoptotic loss, but as a complex erosion of cellular identity termed “dedifferentiation.” Central to this phenotypic shift is the metabolo-epigenetic axis, where mitochondria act [...] Read more.
The progressive decline in functional β-cell mass in Type 2 Diabetes (T2D) is increasingly recognized not as a simple apoptotic loss, but as a complex erosion of cellular identity termed “dedifferentiation.” Central to this phenotypic shift is the metabolo-epigenetic axis, where mitochondria act as the primary sensing hub, transducing nutrient flux into biochemical signals that govern the chromatin landscape. This review synthesizes current evidence on how mitochondrial metabolites—including Acetyl-CoA, α-ketoglutarate, and NAD+—serve as obligatory co-factors for the epigenetic machinery. We explore how chronic metabolic stress triggers a “Systemic epigenetic destabilization,” leading to the loss of lineage-specific markers and the formation of persistent “metabolic scars.” Furthermore, we discuss the clinical implications of these changes, specifically regarding the phenomenon of metabolic memory and the molecular limits of β-cell reversibility. By integrating foundational transcriptional studies with emerging epigenomic data, we propose that targeting the mitochondrial–epigenetic axis offers a strategic window for re-differentiating failing β-cells and restoring glycemic homeostasis. Full article
(This article belongs to the Special Issue The Role of Pancreatic Beta-Cells in Obesity and Type 2 Diabetes)
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23 pages, 2844 KB  
Review
Βeta-Cells: Stress, Identity, Failure and Diabetes
by Yousun An, Nicholas Norris, Donglai Li and Jenny E. Gunton
Cells 2026, 15(5), 475; https://doi.org/10.3390/cells15050475 - 6 Mar 2026
Viewed by 679
Abstract
Type 2 diabetes (T2D) is a pressing global health challenge, primarily driven by modern dietary and lifestyle patterns. Central to T2D progression is the dysfunction of insulin-secreting pancreatic β-cells, which critically disrupts glucose homeostasis. The progression to T2D relies on the β-cells’ inability [...] Read more.
Type 2 diabetes (T2D) is a pressing global health challenge, primarily driven by modern dietary and lifestyle patterns. Central to T2D progression is the dysfunction of insulin-secreting pancreatic β-cells, which critically disrupts glucose homeostasis. The progression to T2D relies on the β-cells’ inability to compensate for increasing insulin resistance. Initially, β-cells enhance the insulin output, but chronic nutrient overload, ER stress and inflammation ultimately compromise their function and survival. This review examines the molecular and cellular drivers of β-cell failure, focusing on endoplasmic reticulum stress, mitochondrial dysfunction and inflammatory pathways amid chronic metabolic stress. We also explore the loss of β-cell identity and altered interactions within the islet microenvironment. Understanding these mechanisms is essential for developing strategies to prevent β-cell dysfunction and slow T2D progression, ultimately supporting better metabolic health outcomes. Full article
(This article belongs to the Special Issue The Role of Pancreatic Beta-Cells in Obesity and Type 2 Diabetes)
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