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Diabetes: Regulation of Insulin Secretion in Pancreatic Beta Cells

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 30 August 2024 | Viewed by 2088

Special Issue Editors


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Guest Editor
1. Biosanitary Research Institute of Granada (ibs.GRANADA), Granada, Spain
2. Centre of Biomedical Research (CIBM), University of Granada, Granada, Spain
Interests: nrf2; renal disease; acute kidney injury; oxidative stress; inflammatory response

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Guest Editor
Weill Department of Medicine, Rockefeller University, New York, NY, USA
Interests: islet; physiology; pathogenesis; type 2 diabetes

Special Issue Information

Dear Colleagues,

The intricate interplay of hormones within the pancreatic islets orchestrates metabolic equilibrium, with pancreatic β cells assuming a central role. These cells, responsible for synthesizing and secreting insulin, play a critical role in controlling plasma glucose levels. The significance of well-functioning pancreatic β cells becomes pronounced given their involvement in the pathogenesis of both type 1 and type 2 diabetes. Recent investigations into the regulation of insulin secretion offer new perspectives. The exploration into the diverse subpopulations of β cells has underscored their distinct functions in shaping insulin secretion dynamics.

This Special Issue of the International Journal of Molecular Sciences (IJMS) delves into molecular mechanisms of insulin secretion and advances in understanding pancreatic β cell failure. We invite innovative contributions elucidating β cell function focusing on the regulation of insulin secretion. Join us in shaping the future of diabetes research.

Dr. Alfonso Rubio-Navarro
Dr. Nicolás Gómez-Banoy
Guest Editors

Manuscript Submission Information

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Keywords

  • beta cells
  • pancreatic islets
  • insulin secretion
  • insulin production
  • diabetes
  • hyperglycemia
  • beta cell heterogeneity

Published Papers (2 papers)

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Research

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13 pages, 979 KiB  
Article
Congenital Hyperinsulinism in Humans and Insulin Secretory Dysfunction in Mice Caused by Biallelic DNAJC3 Variants
by Alena Welters, Oliver Nortmann, Laura Wörmeyer, Clemens Freiberg, Daniel Eberhard, Nadine Bachmann, Carsten Bergmann, Ertan Mayatepek, Thomas Meissner and Sebastian Kummer
Int. J. Mol. Sci. 2024, 25(2), 1270; https://doi.org/10.3390/ijms25021270 - 20 Jan 2024
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Abstract
The BiP co-chaperone DNAJC3 protects cells during ER stress. In mice, the deficiency of DNAJC3 leads to beta-cell apoptosis and the gradual onset of hyperglycemia. In humans, biallelic DNAJC3 variants cause a multisystem disease, including early-onset diabetes mellitus. Recently, hyperinsulinemic hypoglycemia (HH) has [...] Read more.
The BiP co-chaperone DNAJC3 protects cells during ER stress. In mice, the deficiency of DNAJC3 leads to beta-cell apoptosis and the gradual onset of hyperglycemia. In humans, biallelic DNAJC3 variants cause a multisystem disease, including early-onset diabetes mellitus. Recently, hyperinsulinemic hypoglycemia (HH) has been recognized as part of this syndrome. This report presents a case study of an individual with HH caused by DNAJC3 variants and provides an overview of the metabolic phenotype of individuals with HH and DNAJC3 variants. The study demonstrates that HH may be a primary symptom of DNAJC3 deficiency and can persist until adolescence. Additionally, glycemia and insulin release were analyzed in young DNACJ3 knockout (K.O.) mice, which are equivalent to human infants. In the youngest experimentally accessible age group of 4-week-old mice, the in vivo glycemic phenotype was already dominated by a reduced total insulin secretion capacity. However, on a cellular level, the degree of insulin release of DNAJC3 K.O. islets was higher during periods of increased synthetic activity (high-glucose stimulation). We propose that calcium leakage from the ER into the cytosol, due to disrupted DNAJC3-controlled gating of the Sec61 channel, is the most likely mechanism for HH. This is the first genetic mechanism explaining HH solely by the disruption of intracellular calcium homeostasis. Clinicians should screen for HH in DNAJC3 deficiency and consider DNAJC3 variants in the differential diagnosis of congenital hyperinsulinism. Full article
(This article belongs to the Special Issue Diabetes: Regulation of Insulin Secretion in Pancreatic Beta Cells)
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Review

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10 pages, 2347 KiB  
Review
Roles of β-Cell Hypoxia in the Progression of Type 2 Diabetes
by Kazuya Yamagata, Tomonori Tsuyama and Yoshifumi Sato
Int. J. Mol. Sci. 2024, 25(8), 4186; https://doi.org/10.3390/ijms25084186 - 10 Apr 2024
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Abstract
Type 2 diabetes is a chronic disease marked by hyperglycemia; impaired insulin secretion by pancreatic β-cells is a hallmark of this disease. Recent studies have shown that hypoxia occurs in the β-cells of patients with type 2 diabetes and hypoxia, in turn, contributes [...] Read more.
Type 2 diabetes is a chronic disease marked by hyperglycemia; impaired insulin secretion by pancreatic β-cells is a hallmark of this disease. Recent studies have shown that hypoxia occurs in the β-cells of patients with type 2 diabetes and hypoxia, in turn, contributes to the insulin secretion defect and β-cell loss through various mechanisms, including the activation of hypoxia-inducible factors, induction of transcriptional repressors, and activation of AMP-activated protein kinase. This review focuses on advances in our understanding of the contribution of β-cell hypoxia to the development of β-cell dysfunction in type 2 diabetes. A better understanding of β-cell hypoxia might be useful in the development of new strategies for treating type 2 diabetes. Full article
(This article belongs to the Special Issue Diabetes: Regulation of Insulin Secretion in Pancreatic Beta Cells)
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