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Metabolic and Functional Specializations of Pancreatic Beta Cell
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Metabolic and Functional Specializations of Pancreatic Beta Cell

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: closed (31 December 2023) | Viewed by 2784

Special Issue Editor

Prof. Dr. Ingo Rustenbeck

E-Mail Website
Guest Editor
Institute of Pharmacology, Toxicology and Clinical Pharmacy, Technische Universität Braunschweig, D-38106 Braunschweig, Germany
Interests: diabetes; biphasic kinetic of insulin secretion; glucose homeostasis; insulin secretion; pancreas islet beta cell; glucose

Special Issue Information

Dear Colleagues,

Despite intensive research activities in the area of stimulus–secretion coupling in the pancreatic beta-cell, many open questions remain. One may even feel that with the increased amount of data available, the number of controversial issues has increased, e.g., it has been questioned whether the rise of the ATP/ADP ratio in cytosol during glucose stimulation really results from the increased activity of the oxidative phosphorylation. In addition, it has been argued that cataplerosis, which is apparently intimately linked to the stimulus–secretion coupling of the beta-cell, does not involve the export of citrate, which was originally believed to be firmly established. Apparently, the function of the beta-cell mitochondria is more complex and less well-understood than current textbook knowledge suggests.

For the present Special Issue of IJMS, manuscripts exploring the mitochondrial metabolism during the physiological and pathophysiological regulation of insulin secretion, with an emphasis on processes specific to the beta-cell, are invited. In other words, what sets the beta-cell apart from other endocrine islet cells? Specifically, topics of interest include, but are not restricted to, the following:

  • The tight coupling of glycolysis to the mitochondrial metabolism: how important are the glycerophosphate and malate–aspartate shuttle systems?
  • Pyruvate-dehydrogenase and -carboxylase gene expression and activity: why does the beta cell need pyruvate carboxylase?
  • GABA synthesis in the beta cell: are the GABA shunt and its enzymes (glutamic acid decarboxylase = GAD65, GABA transaminase, and semialdehyde succinic acid dehydrogenase) only needed to exert paracrine inhibition?
  • Is GABA shunt metabolism conditioning mitochondrial ATP production via the glucose metabolism in the citric acid cycle?
  • Mitochondrial signaling to exocytosis beyond the ATP/ADP ratio: it exists, but through which signals and which mechanisms?
  • Mitochondrial structure: how important are fusion/fission and mitophagy for beta-cell signal transduction?
  • The role of fatty acids in the beta-cell: when is the beta-oxidation active and what are the consequences?

The editors believe that these very basic topics can be addressed in insulin-secreting cell lines as well as in primary beta cells and islets from rodents and humans.

Prof. Dr. Ingo Rustenbeck
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • pancreatic β-cells
  • tumoral β-cells
  • insulin secretion
  • pyruvate-dehydrogenase
  • pyruvate-carboxylase
  • cataplerosis
  • GABA shunt
  • mitochondrial metabolism
  • β-cell models

Published Papers (2 papers)

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Research

18 pages, 6826 KiB  
Article
Short-Term Inhibition of Translation by Cycloheximide Concurrently Affects Mitochondrial Function and Insulin Secretion in Islets from Female Mice
by Mohammed Alshafei, Torben Schulze, Mai Morsi, Uwe Panten and Ingo Rustenbeck
Int. J. Mol. Sci. 2023, 24(20), 15464; https://doi.org/10.3390/ijms242015464 - 23 Oct 2023
Viewed by 962
Abstract
Since glucose stimulates protein biosynthesis in beta cells concomitantly with the stimulation of insulin release, the possible interaction of both processes was explored. The protein biosynthesis was inhibited by 10 μM cycloheximide (CHX) 60 min prior to the stimulation of perifused, freshly isolated [...] Read more.
Since glucose stimulates protein biosynthesis in beta cells concomitantly with the stimulation of insulin release, the possible interaction of both processes was explored. The protein biosynthesis was inhibited by 10 μM cycloheximide (CHX) 60 min prior to the stimulation of perifused, freshly isolated or 22 h-cultured NMRI mouse islets. CHX reduced the insulinotropic effect of 25 mM glucose or 500 μM tolbutamide in fresh but not in cultured islets. In cultured islets the second phase of glucose stimulation was even enhanced. In fresh and in cultured islets CHX strongly reduced the content of proinsulin, but not of insulin, and moderately diminished the [Ca2+]i increase during stimulation. The oxygen consumption rate (OCR) of fresh islets was about 50% higher than that of cultured islets at basal glucose and was significantly increased by glucose but not tolbutamide. In fresh, but not in cultured, islets CHX diminished the glucose-induced OCR increase and changes in the NAD(P)H- and FAD-autofluorescence. It is concluded that short-term CHX exposure interferes with the signal function of the mitochondria, which have different working conditions in fresh and in cultured islets. The interference may not be an off-target effect but may result from the inhibited cytosolic synthesis of mitochondrial proteins. Full article
(This article belongs to the Special Issue Metabolic and Functional Specializations of Pancreatic Beta Cell)
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13 pages, 2812 KiB  
Article
Vitamin B12-Induced Autophagy Alleviates High Glucose-Mediated Apoptosis of Islet β Cells
by Yu Zhang, Ling Chu, Xi’an Zhou, Tingxia Xu, Qingwu Shen, Tao Li and Yanyang Wu
Int. J. Mol. Sci. 2023, 24(20), 15217; https://doi.org/10.3390/ijms242015217 - 16 Oct 2023
Cited by 1 | Viewed by 1368
Abstract
High glucose levels can lead to the apoptosis of islet β cells, while autophagy can provide cytoprotection and promote autophagic cell death. Vitamin B12, a water-soluble B vitamin, has been shown to regulate insulin secretion and increase insulin sensitivity. However, the precise mechanism [...] Read more.
High glucose levels can lead to the apoptosis of islet β cells, while autophagy can provide cytoprotection and promote autophagic cell death. Vitamin B12, a water-soluble B vitamin, has been shown to regulate insulin secretion and increase insulin sensitivity. However, the precise mechanism of action remains unclear. In this study, we investigated the influence of vitamin B12 on high glucose-induced apoptosis and autophagy in RIN-m5F cells to elucidate how vitamin B12 modulates insulin release. Our results demonstrate that exposure to 45 mM glucose led to a significant increase in the apoptosis rate of RIN-m5F cells. The treatment with vitamin B12 reduced the apoptosis rate and increased the number of autophagosomes. Moreover, vitamin B12 increased the ratio of microtubule-associated protein 1 light chain 3 beta to microtubule-associated protein 1 light chain 3 alpha (LC3-II/LC3-I), while decreasing the amount of sequestosome 1 (p62) and inhibiting the phosphorylation of p70 ribosomal protein S6 kinase (p70S6K) under both normal- and high-glucose conditions. The additional experiments revealed that vitamin B12 inhibited high glucose-induced apoptosis. Notably, this protective effect was attenuated when the autophagy inhibitor 3-methyladenine was introduced. Our findings suggest that vitamin B12 protects islet β cells against apoptosis induced by high glucose levels, possibly by inducing autophagy. Full article
(This article belongs to the Special Issue Metabolic and Functional Specializations of Pancreatic Beta Cell)
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