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New Advances in Cellular and Molecular Biology of the Pancreatic...
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New Advances in Cellular and Molecular Biology of the Pancreatic Beta Cell

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (31 December 2022) | Viewed by 12538

Special Issue Editor

Dr. Jean Sébastien Annicotte

E-Mail Website1 Website2
Guest Editor
Université de Lille, Inserm, CHU Lille, Institut Pasteur de Lille, U1167 – RID-AGE-Facteurs de risque et déterminants moléculaires des maladies liées au vieillissement, F-59000 Lille, France
Interests: pancreatic beta cell; metabolic homeostasis; type 2 diabetes; insulin secretion; insulin resistance; epigenetic regulations; cell cycle regulators
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Insulin-producing pancreatic β-cells play a crucial role in maintaining glucose homeostasis. Type 2 Diabetes (T2D) is characterized by high blood glucose levels and develops due to inadequate pancreatic β-cell function (i.e., insulin secretion) in the face of peripheral insulin resistance of metabolic tissues such as liver, muscle or adipose tissue. In the context of T2D research, several studies have revealed that β-cell dysfunction is thought to have a major role in the pathogenesis of T2D. The restoration of normal β-cell mass and function has therefore become a field of intensive research seeking the next generation of antidiabetic drugs.

Metabolic (dys)homeostasis is controlled by fine-tuned and non-permanent modulations of gene expression in response to extracellular stimuli. This allows the cells to adapt to their environment to maintain cell integrity in response to metabolic challenges. Among the factors that impact the disease, obesity, physical inactivity, and aging are considered non-genetic risk factors contributing to T2D development. These environmental factors have been reported to shape subtle and reversible cellular and molecular events, including, but not limited to, modifications of DNA, named epigenetic regulations, or RNA, named epitrancriptomic regulations, influencing gene transcription and organ dysfunction. In addition, inter-organ crosstalk is a crucial element in determining proper or altered β-cell mass and function. Although the mechanisms underlying β-cell dysfunction are still debated, emerging data suggest that specific molecular and cellular effects are necessary for β-cell adaptation to metabolic stress.

The aim of this Special Issue is to provide an overview of the recent advances in molecular and cellular cues involved in the control of β-cell mass and/or function and propose an integrated view of the biological effects that could contribute at the β-cell level to metabolic disorders, such as T2D. This Special Issue welcomes mechanistic studies investigating the loss of β-cell mass and/or function in the context of T2D and crosstalk of pancreatic islets with other metabolic organs. We hope that the original research and reviews presented by expert laboratories will be valuable to improve our knowledge of the fascinating β-cell and provide new concepts to prevent or propose new treatment strategies to counteract β-cell failure.

Dr. Jean Sébastien Annicotte
Guest Editor

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Keywords

  • pancreatic beta cells
  • type 2 diabetes
  • insulin secretion
  • beta cell adaptation
  • beta cell mass
  • beta cell omics
  • inter-organ crosstalk

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Published Papers (4 papers)

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Research

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14 pages, 2394 KiB  
Article
High-Throughput Quantitative Screening of Glucose-Stimulated Insulin Secretion and Insulin Content Using Automated MALDI-TOF Mass Spectrometry
by Clément Philippe Delannoy, Egon Heuson, Adrien Herledan, Frederik Oger, Bryan Thiroux, Mickaël Chevalier, Xavier Gromada, Laure Rolland, Philippe Froguel, Benoit Deprez, Sébastien Paul and Jean-Sébastien Annicotte
Cells 2023, 12(6), 849; https://doi.org/10.3390/cells12060849 - 9 Mar 2023
Cited by 3 | Viewed by 2460
Abstract
Type 2 diabetes (T2D) is a metabolic disorder characterized by loss of pancreatic β-cell function, decreased insulin secretion and increased insulin resistance, that affects more than 537 million people worldwide. Although several treatments are proposed to patients suffering from T2D, long-term control of [...] Read more.
Type 2 diabetes (T2D) is a metabolic disorder characterized by loss of pancreatic β-cell function, decreased insulin secretion and increased insulin resistance, that affects more than 537 million people worldwide. Although several treatments are proposed to patients suffering from T2D, long-term control of glycemia remains a challenge. Therefore, identifying new potential drugs and targets that positively affect β-cell function and insulin secretion remains crucial. Here, we developed an automated approach to allow the identification of new compounds or genes potentially involved in β-cell function in a 384-well plate format, using the murine β-cell model Min6. By using MALDI-TOF mass spectrometry, we implemented a high-throughput screening (HTS) strategy based on the automation of a cellular assay allowing the detection of insulin secretion in response to glucose, i.e., the quantitative detection of insulin, in a miniaturized system. As a proof of concept, we screened siRNA targeting well-know β-cell genes and 1600 chemical compounds and identified several molecules as potential regulators of insulin secretion and/or synthesis, demonstrating that our approach allows HTS of insulin secretion in vitro. Full article
(This article belongs to the Special Issue New Advances in Cellular and Molecular Biology of the Pancreatic Beta Cell)
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19 pages, 7709 KiB  
Article
Pancreatic Islet Cells Response to IFNγ Relies on Their Spatial Location within an Islet
by Marine De Burghgrave, Chloé Lourenço, Claire Berthault, Virginie Aiello, Adrian Villalba, Alexis Fouque, Marc Diedisheim, Sylvaine You, Masaya Oshima and Raphaël Scharfmann
Cells 2023, 12(1), 113; https://doi.org/10.3390/cells12010113 - 28 Dec 2022
Cited by 2 | Viewed by 3700
Abstract
Type 1 diabetes (T1D) is an auto-immune disease characterized by the progressive destruction of insulin-producing pancreatic beta cells. While beta cells are the target of the immune attack, the other islet endocrine cells, namely the alpha and delta cells, can also be affected [...] Read more.
Type 1 diabetes (T1D) is an auto-immune disease characterized by the progressive destruction of insulin-producing pancreatic beta cells. While beta cells are the target of the immune attack, the other islet endocrine cells, namely the alpha and delta cells, can also be affected by the inflammatory milieu. Here, using a flow cytometry-based strategy, we compared the impact of IFNγ, one of the main cytokines involved in T1D, on the three endocrine cell subsets isolated from C57BL/6 mouse islets. RNA-seq analyses revealed that alpha and delta cells exposed in vitro to IFNγ display a transcriptomic profile very similar to that of beta cells, with an increased expression of inflammation key genes such as MHC class I molecules, the CXCL10 chemokine and the programmed death-ligand 1 (PD-L1), three hallmarks of IFNγ signaling. Interestingly, at low IFNγ concentration, we observed two beta cell populations (responders and non-responders) based on PD-L1 protein expression. Our data indicate that this differential sensitivity relies on the location of the cells within the islet rather than on the existence of two different beta cells subsets. The same findings were corroborated by the in vivo analysis of pancreatic islets from the non-obese diabetic mouse model of T1D, showing more intense PD-L1 staining on endocrine cells close to immune infiltrate. Collectively, our work demonstrates that alpha and delta cells are as sensitive as beta cells to IFNγ, and suggests a gradual diffusion of the cytokine into an islet. These observations provide novel insights into the in situ inflammatory processes occurring in T1D progression. Full article
(This article belongs to the Special Issue New Advances in Cellular and Molecular Biology of the Pancreatic Beta Cell)
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19 pages, 3230 KiB  
Article
Pseudoislet Aggregation of Pancreatic β-Cells Improves Glucose Stimulated Insulin Secretion by Altering Glucose Metabolism and Increasing ATP Production
by Deborah Cornell, Satomi Miwa, Merilin Georgiou, Scott James Anderson, Minna Honkanen-Scott, James A. M. Shaw and Catherine Arden
Cells 2022, 11(15), 2330; https://doi.org/10.3390/cells11152330 - 29 Jul 2022
Cited by 5 | Viewed by 3005
Abstract
Appropriate glucose-stimulated insulin secretion (GSIS) by pancreatic β-cells is an essential component of blood glucose homeostasis. Configuration of β-cells as 3D pseudoislets (PI) improves the GSIS response compared to 2D monolayer (ML) culture. The aim of this study was to determine the underlying [...] Read more.
Appropriate glucose-stimulated insulin secretion (GSIS) by pancreatic β-cells is an essential component of blood glucose homeostasis. Configuration of β-cells as 3D pseudoislets (PI) improves the GSIS response compared to 2D monolayer (ML) culture. The aim of this study was to determine the underlying mechanisms. MIN6 β-cells were grown as ML or PI for 5 days. Human islets were isolated from patients without diabetes. Function was assessed by GSIS and metabolic capacity using the Seahorse bioanalyser. Connexin 36 was downregulated using inducible shRNA. Culturing MIN6 as PI improved GSIS. MIN6 PI showed higher glucose-stimulated oxygen consumption (OCR) and extracellular acidification (ECAR) rates. Further analysis showed the higher ECAR was, at least in part, a consequence of increased glycolysis. Intact human islets also showed glucose-stimulated increases in both OCR and ECAR rates, although the latter was smaller in magnitude compared to MIN6 PI. The higher rates of glucose-stimulated ATP production in MIN6 PI were consistent with increased enzyme activity of key glycolytic and TCA cycle enzymes. There was no impact of connexin 36 knockdown on GSIS or ATP production. Configuration of β-cells as PI improves GSIS by increasing the metabolic capacity of the cells, allowing higher ATP production in response to glucose. Full article
(This article belongs to the Special Issue New Advances in Cellular and Molecular Biology of the Pancreatic Beta Cell)
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Review

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13 pages, 3010 KiB  
Review
Wnt Pathway in Pancreatic Development and Pathophysiology
by Tiziana Napolitano, Serena Silvano, Chaïma Ayachi, Magali Plaisant, Anette Sousa-Da-Veiga, Hugo Fofo, Benjamin Charles and Patrick Collombat
Cells 2023, 12(4), 565; https://doi.org/10.3390/cells12040565 - 9 Feb 2023
Cited by 7 | Viewed by 2734
Abstract
The pancreas is an abdominal gland that serves 2 vital purposes: assist food processing by secreting digestive enzymes and regulate blood glucose levels by releasing endocrine hormones. During embryonic development, this gland originates from epithelial buds located on opposite sites of the foregut [...] Read more.
The pancreas is an abdominal gland that serves 2 vital purposes: assist food processing by secreting digestive enzymes and regulate blood glucose levels by releasing endocrine hormones. During embryonic development, this gland originates from epithelial buds located on opposite sites of the foregut endoderm. Pancreatic cell specification and maturation are coordinated by a complex interplay of extrinsic and intrinsic signaling events. In the recent years, the canonical Wnt/β-catenin pathway has emerged as an important player of pancreas organogenesis, regulating pancreatic epithelium specification, compartmentalization and expansion. Importantly, it has been suggested to regulate proliferation, survival and function of adult pancreatic cells, including insulin-secreting β-cells. This review summarizes recent work on the role of Wnt/β-catenin signaling in pancreas biology from early development to adulthood, emphasizing on its relevance for the development of new therapies for pancreatic diseases. Full article
(This article belongs to the Special Issue New Advances in Cellular and Molecular Biology of the Pancreatic Beta Cell)
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