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β-Cells at the Center of Type 1 and Type 2...
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β-Cells at the Center of Type 1 and Type 2 Diabetes

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (30 September 2024) | Viewed by 6581

Special Issue Editor

Dr. Jeffery S. Tessem

E-Mail Website
Guest Editor
Nutrition, Dietetics and Food Science Department, Brigham Young University, Provo, UT 84602, USA
Interests: beta cell; insulin secretion; cell cycle; mitochondrial respiration;nuclear hormone receptors; Nr4a1; Nr4a3

Special Issue Information

Dear Colleagues, 

Damage to and the failure of pancreatic beta cells are central to type 1 and type 2 diabetes. Impaired insulin secretion, insufficient proliferation, increased cell death, and dedifferentiation lead to impaired functional beta cell mass, which is central to T1D and T2D disease progression. Our understanding of the mechanisms and function of the beta cell under healthy and diseased conditions, as well as across the life cycle, has greatly expanded. Studies focusing on function, survival, replication, structure, epigenetics, and “omics” data have begun to help us understand the central role that the beta cell has in T1D and T2D. This Special Issue aims to highlight the changes to the beta cell across both T1D and T2D, as well as throughout the lifespan. In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: beta cell mass, beta cell function, beta cell signaling, beta cell death, beta cell ER stress, glucolipotoxicity and the beta cell, and beta cell dedifferention.

We look forward to receiving your contributions.

Dr. Jeffery S. Tessem
Guest Editor

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Keywords

  • beta cell
  • insulin secretion
  • cell cycle
  • mitochondrial respiration
  • nuclear hormone receptors
  • Nr4a1
  • Nr4a3

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Published Papers (4 papers)

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Research

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18 pages, 4101 KiB  
Article
Maternal Low-Protein Diet During Nursing Leads to Glucose–Insulin Dyshomeostasis and Pancreatic-Islet Dysfunction by Disrupting Glucocorticoid Responsiveness in Male Rats
by Paulo Cezar de Freitas Mathias, Aline Milena Dantas Rodrigues, Patrícia Cristina Lisboa, Rosiane Aparecida Miranda, Ananda Malta, Tatiane Aparecida Ribeiro, Luiz Felipe Barella, Ginislene Dias, Thalyne Aparecida Leite Lima, Rodrigo Mello Gomes, Egberto Gaspar de Moura and Júlio Cezar de Oliveira
Biology 2024, 13(12), 1036; https://doi.org/10.3390/biology13121036 - 11 Dec 2024
Viewed by 334
Abstract
Both perinatal malnutrition and elevated glucocorticoids are pivotal triggers of the growing global pandemic of metabolic diseases. Here, we studied the effects of metabolic stress responsiveness on glucose–insulin homeostasis and pancreatic-islet function in male Wistar offspring whose mothers underwent protein restriction during lactation. [...] Read more.
Both perinatal malnutrition and elevated glucocorticoids are pivotal triggers of the growing global pandemic of metabolic diseases. Here, we studied the effects of metabolic stress responsiveness on glucose–insulin homeostasis and pancreatic-islet function in male Wistar offspring whose mothers underwent protein restriction during lactation. During the first two weeks after delivery, lactating dams were fed a low-protein (4% protein, LP group) or normal-protein diet (22.5% protein, NP group). At 90 days of age, male rat offspring were challenged with food deprivation (72 h of fasting), intracerebroventricular (icv) injection of dexamethasone (2 µL, 2.115 mmol/L) or chronic intraperitoneal injection of dexamethasone (1 mg/kg body weight/5 days). Body weight, food intake, intravenous glucose tolerance test (ivGTT) results, insulin secretion and biochemical parameters were assessed. LP rats did not display significant metabolic changes after long-term starvation (p > 0.05) or under the central effect of dexamethasone (p = 0.999). Chronic dexamethasone induced rapid hyperglycemia (~1.2-fold, p < 0.001) and hyperinsulinemia (NP: 65%; LP: 216%; p < 0.001), decreased insulin sensitivity (NP: ~2-fold; LP: ~4-fold; p < 0.001), reduced insulinemia (20%) and increased glycemia (35%) only in NP rats under ivGTT conditions (p < 0.001). Glucose and acetylcholine insulinotropic effects, as well as the muscarinic receptor antagonist response, were reduced by chronic dexamethasone only in pancreatic islets from NP rats (p < 0.05). The direct effect of dexamethasone on pancreatic islets reduced insulin secretion (NP: 60.2%, p < 0.001; LP: 33.8%, p < 0.001). Peripheral glucose–insulin dyshomeostasis and functional failure of pancreatic islets in LP rats, as evidenced by an impaired acute and chronic response to metabolic stress, may be due to excessive corticosterone action as a long-term consequence. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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15 pages, 3378 KiB  
Article
CEBPA Overexpression Enhances β-Cell Proliferation and Survival
by Peter N. Ellsworth, Jacob A. Herring, Aaron H. Leifer, Jason D. Ray, Weston S. Elison, Peter Daniel Poulson, Jacqueline E. Crabtree, Pam M. Van Ry and Jeffery S. Tessem
Biology 2024, 13(2), 110; https://doi.org/10.3390/biology13020110 - 9 Feb 2024
Cited by 2 | Viewed by 2371
Abstract
A commonality between type 1 and type 2 diabetes is the decline in functional β-cell mass. The transcription factor Nkx6.1 regulates β-cell development and is integral for proper β-cell function. We have previously demonstrated that Nkx6.1 depends on c-Fos mediated upregulation and the [...] Read more.
A commonality between type 1 and type 2 diabetes is the decline in functional β-cell mass. The transcription factor Nkx6.1 regulates β-cell development and is integral for proper β-cell function. We have previously demonstrated that Nkx6.1 depends on c-Fos mediated upregulation and the nuclear hormone receptors Nr4a1 and Nr4a3 to increase β-cell insulin secretion, survival, and replication. Here, we demonstrate that Nkx6.1 overexpression results in upregulation of the bZip transcription factor CEBPA and that CEBPA expression is independent of c-Fos regulation. In turn, CEBPA overexpression is sufficient to enhance INS-1 832/13 β-cell and primary rat islet proliferation. CEBPA overexpression also increases the survival of β-cells treated with thapsigargin. We demonstrate that increased survival in response to ER stress corresponds with changes in expression of various genes involved in the unfolded protein response, including decreased Ire1a expression. These data show that CEBPA is sufficient to enhance functional β-cell mass by increasing β-cell proliferation and modulating the unfolded protein response. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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15 pages, 2212 KiB  
Article
Toll-like Receptor 9 Gene in the Development of Type 2 Diabetes Mellitus in the Saudi Arabian Population
by Zeina S. Alkudmani, Aminah Ahmad Alzailai, Khaled H. Aburisheh, Amal F. Alshammary and Imran Ali Khan
Biology 2023, 12(11), 1439; https://doi.org/10.3390/biology12111439 - 16 Nov 2023
Cited by 2 | Viewed by 1732
Abstract
Diabetes mellitus is a complex disease with a wide range of manifestations. Diabetes, notably type 2 diabetes mellitus (T2DM), is becoming more common in Saudi Arabia as a result of obesity and an aging population. T2DM is classified as a noncommunicable disease, and [...] Read more.
Diabetes mellitus is a complex disease with a wide range of manifestations. Diabetes, notably type 2 diabetes mellitus (T2DM), is becoming more common in Saudi Arabia as a result of obesity and an aging population. T2DM is classified as a noncommunicable disease, and its incidence in the Saudi population continues to grow as a consequence of socioeconomic changes. Toll-like receptors (TLRs) are innate immune receptors that mediate the inflammatory response in diabetes mellitus. Previous studies have documented the relationship between different SNPs in the TLR9 gene in different forms of diabetes. As a result, the purpose of this study was to investigate the relationship between rs187084, rs352140, and rs5743836 SNPs in the TLR9 gene among T2DM patients in the Saudi population. This was a case-control study that included 100 T2DM cases and 100 control subjects. The three SNPs were identified in the study population (n = 200) using polymerase chain reaction (PCR), restriction enzymes for rs352140, and Sanger sequencing for rs187084 and rs5783836. Next, statistical analyses were performed using various software to determine the association between the SNPs and T2DM. rs187084 and rs5743836 were associated with an increased risk of T2DM development. rs187084 and rs5743836 allelic frequencies were associated with a 3.2 times increased risk of T2DM development (p < 0.05). DBP was associated with T2DM (p = 0.02). rs187084 was associated with TC and HDLc; rs352140 was associated with DBP, HbA1c, and HDLc; rs5743836 was associated with waist (p < 0.05). The CGT haplotype was strongly associated with T2DM (p < 0.003). Gene–gene interaction, graphical presentation, and dendrogram showed the strong association with T2DM patients (p < 0.05). This study concluded that rs187084 and rs5743836 were strongly associated with T2DM in Saudi Arabian patients. This study provides further evidence that SNPs in the TLR9 gene play a significant role in T2DM development in a Saudi community. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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Review

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20 pages, 4718 KiB  
Review
Disrupted Endoplasmic Reticulum Ca2+ Handling: A Harβinger of β-Cell Failure
by Jordyn R. Dobson and David A. Jacobson
Biology 2024, 13(6), 379; https://doi.org/10.3390/biology13060379 - 25 May 2024
Cited by 1 | Viewed by 1461
Abstract
The β-cell workload increases in the setting of insulin resistance and reduced β-cell mass, which occurs in type 2 and type 1 diabetes, respectively. The prolonged elevation of insulin production and secretion during the pathogenesis of diabetes results in β-cell ER stress. The [...] Read more.
The β-cell workload increases in the setting of insulin resistance and reduced β-cell mass, which occurs in type 2 and type 1 diabetes, respectively. The prolonged elevation of insulin production and secretion during the pathogenesis of diabetes results in β-cell ER stress. The depletion of β-cell Ca2+ER during ER stress activates the unfolded protein response, leading to β-cell dysfunction. Ca2+ER is involved in many pathways that are critical to β-cell function, such as protein processing, tuning organelle and cytosolic Ca2+ handling, and modulating lipid homeostasis. Mutations that promote β-cell ER stress and deplete Ca2+ER stores are associated with or cause diabetes (e.g., mutations in ryanodine receptors and insulin). Thus, improving β-cell Ca2+ER handling and reducing ER stress under diabetogenic conditions could preserve β-cell function and delay or prevent the onset of diabetes. This review focuses on how mechanisms that control β-cell Ca2+ER are perturbed during the pathogenesis of diabetes and contribute to β-cell failure. Full article
(This article belongs to the Special Issue β-Cells at the Center of Type 1 and Type 2 Diabetes)
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