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Cells
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Advances in Diabetes Pathophysiology and Treatment
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Advances in Diabetes Pathophysiology and Treatment

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

Deadline for manuscript submissions: 31 October 2024 | Viewed by 7351

Special Issue Editors

Dr. Carla Perego

E-Mail Website
Guest Editor
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy
Interests: adhesion molecules; cellular mechanobiology; mitochondrial dynamics; vesicular trafficking; islet of Langerhans; beta cells differentiation; diabetes mellitus; pancreatic tumors; glia–neuron interactions
Special Issues, Collections and Topics in MDPI journals
Dr. Paolo Magni

E-Mail Website
Guest Editor
Department of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Milan, Italy
Interests: metabolic diseases; obesity and adipokines; insulin resistance and diabetes; cardiovascular disease; atherosclerosis; nutraceuticals; nutrition; metabolic biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The global exponential rise in diabetes mellitus incidence is one of the most challenging health concerns of our time and, as a consequence, exploring new strategies to mitigate its spread is mandatory and urgent.

Diabetes mellitus is a chronic metabolic disorder characterized by fasting hyperglycemia triggered by either insulin insufficiency and/or reduced insulin action on target tissues. In recent years, genetic and “omic” studies have provided novel mechanistic insights into disease pathophysiology and discovered novel promising targets of interventions.

Today, 100 years after the discovery of insulin, the goal of this Special Issue is to provide a forum for promoting a synergy between new research discoveries and the development of approaches for the future of diabetes treatments.

Potential topics include, but are not limited to, novel pathways/approaches targeting β-cell functional mass, incretin axis, glucose uptake and metabolism in the liver, insulin sensitivity in peripheral tissues and immunometabolic mechanisms.

Both original research articles and review articles are welcome.

Dr. Carla Perego
Dr. Paolo Magni
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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 mellitus
  • insulin resistance
  • islet of Langerhans
  • insulin
  • incretin
  • glucose homeostasis
  • (ectopic) adipose tissue
  • adipokines
  • liver
  • diabetes cardiovascular complications

Published Papers (3 papers)

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Research

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17 pages, 4567 KiB  
Article
Bromodomain Protein Inhibition Protects β-Cells from Cytokine-Induced Death and Dysfunction via Antagonism of NF-κB Pathway
by Vinny Negi, Jeongkyung Lee, Varun Mandi, Joseph Danvers, Ruya Liu, Eliana M. Perez-Garcia, Feng Li, Rajaganapati Jagannathan, Ping Yang, Domenic Filingeri, Amit Kumar, Ke Ma, Mousumi Moulik and Vijay K. Yechoor
Cells 2024, 13(13), 1108; https://doi.org/10.3390/cells13131108 - 26 Jun 2024
Viewed by 81
Abstract
Cytokine-induced β-cell apoptosis is a major pathogenic mechanism in type 1 diabetes (T1D). Despite significant advances in understanding its underlying mechanisms, few drugs have been translated to protect β-cells in T1D. Epigenetic modulators such as bromodomain-containing BET (bromo- and extra-terminal) proteins are important [...] Read more.
Cytokine-induced β-cell apoptosis is a major pathogenic mechanism in type 1 diabetes (T1D). Despite significant advances in understanding its underlying mechanisms, few drugs have been translated to protect β-cells in T1D. Epigenetic modulators such as bromodomain-containing BET (bromo- and extra-terminal) proteins are important regulators of immune responses. Pre-clinical studies have demonstrated a protective effect of BET inhibitors in an NOD (non-obese diabetes) mouse model of T1D. However, the effect of BET protein inhibition on β-cell function in response to cytokines is unknown. Here, we demonstrate that I-BET, a BET protein inhibitor, protected β-cells from cytokine-induced dysfunction and death. In vivo administration of I-BET to mice exposed to low-dose STZ (streptozotocin), a model of T1D, significantly reduced β-cell apoptosis, suggesting a cytoprotective function. Mechanistically, I-BET treatment inhibited cytokine-induced NF-kB signaling and enhanced FOXO1-mediated anti-oxidant response in β-cells. RNA-Seq analysis revealed that I-BET treatment also suppressed pathways involved in apoptosis while maintaining the expression of genes critical for β-cell function, such as Pdx1 and Ins1. Taken together, this study demonstrates that I-BET is effective in protecting β-cells from cytokine-induced dysfunction and apoptosis, and targeting BET proteins could have potential therapeutic value in preserving β-cell functional mass in T1D. Full article
(This article belongs to the Special Issue Advances in Diabetes Pathophysiology and Treatment)
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16 pages, 3858 KiB  
Article
Duodenal Dual-Wavelength Photobiomodulation Improves Hyperglycemia and Hepatic Parameters with Alteration of Gut Microbiome in Type 2 Diabetes Animal Model
by Se Hee Min, Jinhee Kwon, Eun-Ju Do, So Hee Kim, Eun Sil Kim, Jin-Yong Jeong, Sang Mun Bae, Sang-Yeob Kim and Do Hyun Park
Cells 2022, 11(21), 3490; https://doi.org/10.3390/cells11213490 - 3 Nov 2022
Cited by 8 | Viewed by 2580
Abstract
Background: Recently, the duodenum has garnered interest for its role in treating metabolic diseases, including type 2 diabetes (T2DM). Multiple sessions of external photobiomodulation (PBM) in previous animal studies suggested it resulted in improved hyperglycemia, glucose intolerance, and insulin resistance with a multifactorial [...] Read more.
Background: Recently, the duodenum has garnered interest for its role in treating metabolic diseases, including type 2 diabetes (T2DM). Multiple sessions of external photobiomodulation (PBM) in previous animal studies suggested it resulted in improved hyperglycemia, glucose intolerance, and insulin resistance with a multifactorial mechanism of action, despite the target organ of PBM not being clearly proven. This study aimed to determine whether a single session of a duodenal light-emitting diode (LED) PBM may impact the T2DM treatment in an animal model. Methods: Goto–Kakizaki rats as T2DM models were subjected to PBM through duodenal lumen irradiation, sham procedure, or control in 1-week pilot (630 nm, 850 nm, or 630/850 nm) and 4-week follow-up (630 nm or 630/850 nm) studies. Oral glucose tolerance tests; serum glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide, and insulin levels; liver chemistry and histology; and gut microbiome in the PBM, sham control, and control groups were evaluated. Results: In the 1-week study, duodenal dual-wavelength (D, 630/850 nm) LED PBM showed improved glucose intolerance, alkaline phosphatase and cholesterol levels, and weight gain than other groups. The D-LED PBM group in the 4-week study also showed improved hyperglycemia and liver enzyme levels, with relatively preserved pancreatic islets and increased serum insulin and GLP-1 levels. Five genera (Bacteroides, Escherichia, Parabacteroides, Allobaculum, and Faecalibaculum) were significantly enriched 1 week after the D-LED PBM. Bacteroides acidifaciens significantly increased, while Lachnospiraceae significantly decreased after 1 week. Conclusion: A single session of D-LED PBM improved hyperglycemia and hepatic parameters through the change of serum insulin, insulin resistance, insulin expression in the pancreatic β-cells, and gut microbiome in T2DM animal models. Full article
(This article belongs to the Special Issue Advances in Diabetes Pathophysiology and Treatment)
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Review

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12 pages, 1378 KiB  
Review
Emerging Anti-Diabetic Drugs for Beta-Cell Protection in Type 1 Diabetes
by Nida Ajmal, Maislin C. Bogart, Palwasha Khan, Ibiagbani M. Max-Harry and Craig S. Nunemaker
Cells 2023, 12(11), 1472; https://doi.org/10.3390/cells12111472 - 25 May 2023
Cited by 2 | Viewed by 3848
Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disorder that damages beta cells in the pancreatic islets of Langerhans and results in hyperglycemia due to the loss of insulin. Exogenous insulin therapy can save lives but does not halt disease progression. Thus, an [...] Read more.
Type 1 diabetes (T1D) is a chronic autoimmune disorder that damages beta cells in the pancreatic islets of Langerhans and results in hyperglycemia due to the loss of insulin. Exogenous insulin therapy can save lives but does not halt disease progression. Thus, an effective therapy may require beta-cell restoration and suppression of the autoimmune response. However, currently, there are no treatment options available that can halt T1D. Within the National Clinical Trial (NCT) database, a vast majority of over 3000 trials to treat T1D are devoted to insulin therapy. This review focuses on non-insulin pharmacological therapies. Many investigational new drugs fall under the category of immunomodulators, such as the recently FDA-approved CD-3 monoclonal antibody teplizumab. Four intriguing candidate drugs fall outside the category of immunomodulators, which are the focus of this review. Specifically, we discuss several non-immunomodulators that may have more direct action on beta cells, such as verapamil (a voltage-dependent calcium channel blocker), gamma aminobutyric acid (GABA, a major neurotransmitter with effects on beta cells), tauroursodeoxycholic acid (TUDCA, an endoplasmic reticulum chaperone), and volagidemab (a glucagon receptor antagonist). These emerging anti-diabetic drugs are expected to provide promising results in both beta-cell restoration and in suppressing cytokine-derived inflammation. Full article
(This article belongs to the Special Issue Advances in Diabetes Pathophysiology and Treatment)
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