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Advances in Molecular Research of Diabetes Mellitus
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Advances in Molecular Research of Diabetes Mellitus

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 (20 January 2025) | Viewed by 5384

Special Issue Editor

Dr. Anastasia Thanopoulou

E-Mail Website
Guest Editor
Faculty of Medicine, National and Kapodistrian University of Athens, 11527 Athens, Greece
Interests: diabetes mellitus; nutrition; metabolism metabolic; syndrome

Special Issue Information

Dear Colleagues,

Over the last few years, we have witnessed a dramatic increase in the incidence and prevalence of diabetes mellitus (DM), one of the most common non-communicable diseases worldwide. Patients mostly suffer from the two major forms of DM, type 1, wherein autoimmunity-driven pancreatic β-cell death results in a lack of insulin, and type 2, characterized by malfunctioning cellular sensing and response to insulin and/or defective insulin secretion, eventually leading to hyperglycaemia. The less common forms, such as monogenic diabetes, mitochondrial diabetes, rare syndrome-associated diabetes, etc., are present in the rest of the patient population. Individuals who exhibit persistent hyperglycaemia may develop systemic complications such as microangiopathy and macroangiopathy, as well as peripheral neuropathy. Longstanding endeavours in this research field have focused on clarifying the pathophysiological mechanisms linked with DM manifestation and progression to explore the natural history of DM and to find targets able to halt its broad-spectrum comorbidities.

As an effort to provide new findings in this field, this Special Issue will be devoted to the molecular basis of diabetes mellitus. We seek high-quality research papers addressing the molecular aspects of every type of DM. Researchers from a wide range of professional backgrounds are welcome to contribute. Original research papers and state-of-the-art reviews will be considered.

Dr. Anastasia Thanopoulou
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

  • insulin resistance
  • adiposity
  • complications
  • genes

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Published Papers (4 papers)

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Research

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11 pages, 2741 KiB  
Article
β-Cell Deletion of Hypoxia-Inducible Factor 1α (HIF-1α) Increases Pancreatic β-Cell Susceptibility to Streptozotocin
by Josephine Yu, Amit Lalwani and Jenny E. Gunton
Int. J. Mol. Sci. 2024, 25(24), 13451; https://doi.org/10.3390/ijms252413451 - 15 Dec 2024
Viewed by 1274
Abstract
Type 1 diabetes (T1D) is caused by the immune-mediated loss of pancreatic β-cells. Hypoxia-inducible factor 1α (HIF-1α) is a transcription factor which is crucial for cellular responses to low oxygen. Here, we investigate the role of β-cell HIF-1α in β-cell death and diabetes [...] Read more.
Type 1 diabetes (T1D) is caused by the immune-mediated loss of pancreatic β-cells. Hypoxia-inducible factor 1α (HIF-1α) is a transcription factor which is crucial for cellular responses to low oxygen. Here, we investigate the role of β-cell HIF-1α in β-cell death and diabetes after exposure to multiple low-dose streptozotocin (MLDS). MDLS triggers auto-immunity in susceptible animal models, such as non-obese diabetic (NOD) mice. These experiments used a novel mouse model with β-cell-specific deletion of HIF-1α on a NOD background (BIN mice). Mice were given 20 mg/kg MLDS for 5 consecutive days. Following MLDS, 100% of BIN mice developed frank diabetes versus 33% of floxed-control (FC) littermates and 17% of NOD controls (p < 0.001). BIN mice had obvious loss of β-cell mass (p < 0.0001) and increased necrotic areas within islets (p < 0.001). To confirm that diabetes was T1D, adoptive transfers of splenocytes from diabetic BIN and FC mice were performed on NOD-SCID (Severe Combined ImmunoDeficiency) recipients. All mice receiving BIN-splenocytes developed frank diabetes, confirming that MLDS induced true T1D. Interestingly, diabetes developed significantly faster in BIN-adoptive transfer mice compared to mice which developed diabetes after receiving an FC-adoptive transfer. These studies demonstrate the importance of β-cell HIF-1α in the preservation of β-cell mass and avoidance of auto-immunity. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetes Mellitus)
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26 pages, 3120 KiB  
Article
Multi-Omics Analysis Revealed the rSNPs Potentially Involved in T2DM Pathogenic Mechanism and Metformin Response
by Igor S. Damarov, Elena E. Korbolina, Elena Y. Rykova and Tatiana I. Merkulova
Int. J. Mol. Sci. 2024, 25(17), 9297; https://doi.org/10.3390/ijms25179297 - 27 Aug 2024
Viewed by 1332
Abstract
The goal of our study was to identify and assess the functionally significant SNPs with potentially important roles in the development of type 2 diabetes mellitus (T2DM) and/or their effect on individual response to antihyperglycemic medication with metformin. We applied a bioinformatics approach [...] Read more.
The goal of our study was to identify and assess the functionally significant SNPs with potentially important roles in the development of type 2 diabetes mellitus (T2DM) and/or their effect on individual response to antihyperglycemic medication with metformin. We applied a bioinformatics approach to identify the regulatory SNPs (rSNPs) associated with allele-asymmetric binding and expression events in our paired ChIP-seq and RNA-seq data for peripheral blood mononuclear cells (PBMCs) of nine healthy individuals. The rSNP outcomes were analyzed using public data from the GWAS (Genome-Wide Association Studies) and Genotype-Tissue Expression (GTEx). The differentially expressed genes (DEGs) between healthy and T2DM individuals (GSE221521), including metformin responders and non-responders (GSE153315), were searched for in GEO RNA-seq data. The DEGs harboring rSNPs were analyzed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG). We identified 14,796 rSNPs in the promoters of 5132 genes of human PBMCs. We found 4280 rSNPs to associate with both phenotypic traits (GWAS) and expression quantitative trait loci (eQTLs) from GTEx. Between T2DM patients and controls, 3810 rSNPs were detected in the promoters of 1284 DEGs. Based on the protein-protein interaction (PPI) network, we identified 31 upregulated hub genes, including the genes involved in inflammation, obesity, and insulin resistance. The top-ranked 10 enriched KEGG pathways for these hubs included insulin, AMPK, and FoxO signaling pathways. Between metformin responders and non-responders, 367 rSNPs were found in the promoters of 131 DEGs. Genes encoding transcription factors and transcription regulators were the most widely represented group and many were shown to be involved in the T2DM pathogenesis. We have formed a list of human rSNPs that add functional interpretation to the T2DM-association signals identified in GWAS. The results suggest candidate causal regulatory variants for T2DM, with strong enrichment in the pathways related to glucose metabolism, inflammation, and the effects of metformin. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetes Mellitus)
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17 pages, 1336 KiB  
Article
The Importance of Molecular Genetic Testing for Precision Diagnostics, Management, and Genetic Counseling in MODY Patients
by Lăcrămioara Ionela Butnariu, Delia Andreia Bizim, Carmen Oltean, Cristina Rusu, Monica Cristina Pânzaru, Gabriela Păduraru, Nicoleta Gimiga, Gabriela Ghiga, Ștefana Maria Moisă, Elena Țarcă, Iuliana Magdalena Starcea, Setalia Popa and Laura Mihaela Trandafir
Int. J. Mol. Sci. 2024, 25(12), 6318; https://doi.org/10.3390/ijms25126318 - 7 Jun 2024
Cited by 1 | Viewed by 1669
Abstract
Maturity-onset diabetes of the young (MODY) is part of the heterogeneous group of monogenic diabetes (MD) characterized by the non-immune dysfunction of pancreatic β-cells. The diagnosis of MODY still remains a challenge for clinicians, with many cases being misdiagnosed as type 1 or [...] Read more.
Maturity-onset diabetes of the young (MODY) is part of the heterogeneous group of monogenic diabetes (MD) characterized by the non-immune dysfunction of pancreatic β-cells. The diagnosis of MODY still remains a challenge for clinicians, with many cases being misdiagnosed as type 1 or type 2 diabetes mellitus (T1DM/T2DM), and over 80% of cases remaining undiagnosed. With the introduction of modern technologies, important progress has been made in deciphering the molecular mechanisms and heterogeneous etiology of MD, including MODY. The aim of our study was to identify genetic variants associated with MODY in a group of patients with early-onset diabetes/prediabetes in whom a form of MD was clinically suspected. Genetic testing, based on next-generation sequencing (NGS) technology, was carried out either in a targeted manner, using gene panels for monogenic diabetes, or by analyzing the entire exome (whole-exome sequencing). GKC-MODY 2 was the most frequently detected variant, but rare forms of KCNJ11-MODY 13, specifically, HNF4A-MODY 1, were also identified. We have emphasized the importance of genetic testing for early diagnosis, MODY subtype differentiation, and genetic counseling. We presented the genotype–phenotype correlations, especially related to the clinical evolution and personalized therapy, also emphasizing the particularities of each patient in the family context. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetes Mellitus)
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Review

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24 pages, 5118 KiB  
Review
Decoding the Contribution of IAPP Amyloid Aggregation to Beta Cell Dysfunction: A Systematic Review and Epistemic Meta-Analysis of Type 1 Diabetes
by Valeria Moya-Gudiño, Nelly F. Altamirano-Bustamante, Cristina Revilla-Monsalve and Myriam M. Altamirano-Bustamante
Int. J. Mol. Sci. 2025, 26(2), 767; https://doi.org/10.3390/ijms26020767 - 17 Jan 2025
Viewed by 337
Abstract
Diabetes Mellitus Type 1 (DM1) is an autoimmune disease characterized by the destruction of beta cells in the pancreas. Although amyloid formation has been well-studied in Diabetes Mellitus Type 2 (DM2), its role in DM1 remains unclear. Understanding how islet amyloid polypeptide (IAPP) [...] Read more.
Diabetes Mellitus Type 1 (DM1) is an autoimmune disease characterized by the destruction of beta cells in the pancreas. Although amyloid formation has been well-studied in Diabetes Mellitus Type 2 (DM2), its role in DM1 remains unclear. Understanding how islet amyloid polypeptide (IAPP) contributes to beta cell dysfunction and death in DM1 could provide critical insights into disease mechanisms and pave the way for novel diagnostic and therapeutic strategies. A systematic review and epistemic meta-analysis was conducted using a modified PICO framework, focusing on studies related to DM1 and the IAPP aggregation process. Searches in PubMed, BIREME, and Web of Science yielded 37 relevant articles, which were analyzed and individually evaluated based on specific quality criteria. Studies that experimentally identified the formation of IAPP oligomers in DM1 were selected, along with relevant review articles. Experimental studies from human and animal models detected the presence of IAPP oligomers in DM1 patients, as well as in nonobese diabetic (NOD) and homozygous mice. Techniques like Western Blot (WB), Transmission Electron Microscopy (TEM) and Congo red staining detected various oligomers sizes, with smaller ones showing higher cytotoxicity. IAPP oligomers have been detected in the pancreatic islets of DM1 patients, contributing to beta cell damage and disease progression. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Diabetes Mellitus)
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