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Biomedicines
Special Issues
Molecular and Cellular Research in Diabetes and Metabolic Diseases
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Molecular and Cellular Research in Diabetes and Metabolic Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Endocrinology and Metabolism Research".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 581

Special Issue Editor

Dr. Miwon Ahn

E-Mail Website
Guest Editor
Department of Molecular and Cellular Endocrinology, Arthur Riggs Diabetes & Metabolism Research Institute, City of Hope Beckman Research Institute, 1500 E. Duarte Rd, Duarte, CA 91010, USA
Interests: beta cell; diet-induced obesity; human islet; type 2 diabetes; pre-diabetes; glucose homeostasis; insulin exocytosis; insulin resistance; organ cross-talk

Special Issue Information

Dear Colleagues,

Type 2 diabetes (T2D) affects approximately 38 million people in the US, with over 98 million having prediabetes. Additionally, the aging population is at risk for developing (pre)T2D. Current antidiabetic drugs have limitations due to their serious side effects and contraindications with certain co-morbidities. While revolutionary anti-obesity drugs such as GLP-1R agonists address a significant portion of the obese population with T2D, they may result in substantial loss in muscle health and mass, which could worsen age-related sarcopenia and pose a safety risk for the aging population susceptible to T2D.

Skeletal muscle insulin resistance contributes to islet β-cell dysfunction in obesity-related T2D, but different populations exhibit varying degrees of insulin secretory capacity and IR. For instance, there is a high incidence of (pre)T2D in lean non-white populations with a BMI < 25, and these individuals often exhibit insulin dysfunction/deficiency rather than IR. This highlights the unmet need for additional safe and effective therapies for (pre)T2D.

Insulin secretion dysfunction and peripheral insulin resistance are key features of metabolic imbalance in prediabetes. Therefore, this Special Issue of Biomedicines focusing on molecular and cellular research in diabetes and metabolic diseases aims to address the gaps in knowledge to better understand diabetes. Our goal in publishing this issue is to promote research and clinical interest in this field, with the hope of understanding the signaling and exocytosis mechanisms that can be modulated to prevent or reverse prediabetes.

Dr. Miwon Ahn
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • insulin exocytosis
  • pre-diabetes
  • type 2 diabetes
  • organ cross-talk
  • diabetes drugs
  • diabetes clinical study
  • glucose homeostasis

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Published Papers (1 paper)

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17 pages, 5511 KiB  
Article
Distinct Roles of apoE Receptor-2 Cytoplasmic Domain Splice Variants in Cardiometabolic Disease Modulation
by Anja Jaeschke, April Haller and David Y. Hui
Biomedicines 2025, 13(7), 1692; https://doi.org/10.3390/biomedicines13071692 - 10 Jul 2025
Viewed by 258
Abstract
Background/Objectives: Apolipoprotein E receptor-2 (apoER2) exists in various alternatively spliced forms, including variants that express apoER2 with or without exon 19 in the cytoplasmic domain. This study compared vascular response to endothelial denudation, as well as diet-induced atherosclerotic and metabolic diseases, between [...] Read more.
Background/Objectives: Apolipoprotein E receptor-2 (apoER2) exists in various alternatively spliced forms, including variants that express apoER2 with or without exon 19 in the cytoplasmic domain. This study compared vascular response to endothelial denudation, as well as diet-induced atherosclerotic and metabolic diseases, between genetically modified mice that exclusively expressed the apoER2 splice variant with or without exon 19 to determine the impact of apoER2 exon 19 motif in cardiometabolic disease modulation. Methods: Vascular response to injury was assessed by measuring neointima area of the carotid arteries after endothelial denudation. The genetically modified mice were also fed a high-fat high-cholesterol diet for 16 weeks for the determination of body weight gain, glucose and insulin levels, glucose tolerance and insulin secretion. Additionally, adipose tissue inflammation was assessed by analysis of adipose gene expression, and atherosclerosis was characterized by measuring fatty lesion size in the whole aorta, as well as in the aortic roots. Results: The results showed that whereas the expression of either splice variant is sufficient to impede denudation-induced fibrotic neointima formation and complex necrotic atherosclerotic lesions, the expression of the apoER2 splice variant containing exon 19 is necessary for the complete protection of injury-induced neointima formation in the vessel wall. However, exclusive expression of either apoER2 cytoplasmic splice variant does not influence the early phase of atherogenesis. Additionally, the exclusive expression of apoER2 without exon 19 promotes adipocyte inflammation and accelerates diet-induced insulin resistance and glucose intolerance. Conclusions: These results indicate that the apoER2 cytoplasmic variants have distinct and cell type-specific roles in influencing cardiometabolic disease development. Full article
(This article belongs to the Special Issue Molecular and Cellular Research in Diabetes and Metabolic Diseases)
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