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Molecular Research on Diabetes

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: 31 August 2024 | Viewed by 3870

Special Issue Editors


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Guest Editor
Department of Internal Medicine and Medical Specialties, University of Genoa, 6 Viale Benedetto XV, 16132 Genoa, Italy
Interests: diabetes; retinopathy; VEGF-A; IGF-1; advanced glycation end-products
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Internal Medicine and Medical Specialties, University of Genova, 16132 Genova, Italy
Interests: the role of caveoles in the insulin and IGF1 signal; new technologies in the treatment of diabetes mellitus; role of bariatric surgery in the regulation of metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetes is a metabolic disease characterized by hyperglycemia. This chronic disorder raises the risk of microvascular as well as neurological disorders and contributes to the pathophysiology of diabetes complications. Type II diabetes accounts for 85–90% of all diabetic patients. There are a range of reasons as to why diabetes can occur: insulin resistance and β cell dysfunction are the main causative abnormalities; however, several mutations in the genes important for glucose homeostasis and β cell development have been related to the progress of hyperglycemia. In addition, environmental factors may influence the incidence of hyperglycemia. Although several studies have aimed to elucidate the molecular mechanisms underlying the development of diabetes and its complications, their precise pathophysiology is not completely understood. This Special Issue aims to collect the latest research on different biological processes and molecular mechanisms that cause diabetes, with a special emphasis on 1. insulin deficiency and insulin resistance, 2. impaired signaling pathways involved in glucose metabolism, 3. glucose transport and defects in transport activity, 4. post-translational modifications of the proteins involved in metabolism, 5. genetic defects associated with diabetes, 6. oxidative stress, and 7. pharmacological agents regulating glucose metabolism.

Dr. Alessandra Puddu
Dr. Davide Maggi
Guest Editors

Manuscript Submission Information

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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.

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Keywords

  • diabetes
  • insulin
  • glucose metabolism
  • oxidative stress

Published Papers (3 papers)

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Research

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15 pages, 2147 KiB  
Article
Low-Density Neutrophils Contribute to Subclinical Inflammation in Patients with Type 2 Diabetes
by Benjamin L. Dumont, Paul-Eduard Neagoe, Elcha Charles, Louis Villeneuve, Jean-Claude Tardif, Agnès Räkel, Michel White and Martin G. Sirois
Int. J. Mol. Sci. 2024, 25(3), 1674; https://doi.org/10.3390/ijms25031674 - 30 Jan 2024
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Abstract
Type 2 diabetes (T2D) is characterized by low-grade inflammation. Low-density neutrophils (LDNs) represent normally less than 2% of total neutrophils but increase in multiple pathologies, releasing inflammatory cytokines and neutrophil extracellular traps (NETs). We assessed the count and role of high-density neutrophils (HDNs), [...] Read more.
Type 2 diabetes (T2D) is characterized by low-grade inflammation. Low-density neutrophils (LDNs) represent normally less than 2% of total neutrophils but increase in multiple pathologies, releasing inflammatory cytokines and neutrophil extracellular traps (NETs). We assessed the count and role of high-density neutrophils (HDNs), LDNs, and NET-related activities in patients with T2D. HDNs and LDNs were purified by fluorescence-activated cell sorting (FACS) and counted by flow cytometry. Circulating inflammatory and NETs biomarkers were measured by ELISA (Enzyme Linked Immunosorbent Assay). NET formation was quantified by confocal microscopy. Neutrophil adhesion onto a human extracellular matrix (hECM) was assessed by optical microscopy. We recruited 22 healthy volunteers (HVs) and 18 patients with T2D. LDN counts in patients with diabetes were significantly higher (160%), along with circulating NETs biomarkers (citrullinated H3 histone (H3Cit), myeloperoxidase (MPO), and MPO-DNA (137%, 175%, and 69%, respectively) versus HV. Circulating interleukins (IL-6 and IL-8) and C-Reactive Protein (CRP) were significantly increased by 117%, 171%, and 79%, respectively, in patients compared to HVs. Isolated LDNs from patients expressed more H3Cit, MPO, and NETs, formed more NETs, and adhered more on hECM compared to LDNs from HVs. Patients with T2D present higher levels of circulating LDN- and NET-related biomarkers and associated pro-inflammatory activities. Full article
(This article belongs to the Special Issue Molecular Research on Diabetes)
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16 pages, 1340 KiB  
Review
Mechanisms and Physiological Roles of Polymorphisms in Gestational Diabetes Mellitus
by Sarocha Suthon and Watip Tangjittipokin
Int. J. Mol. Sci. 2024, 25(4), 2039; https://doi.org/10.3390/ijms25042039 - 7 Feb 2024
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Abstract
Gestational diabetes mellitus (GDM) is a significant pregnancy complication linked to perinatal complications and an elevated risk of future metabolic disorders for both mothers and their children. GDM is diagnosed when women without prior diabetes develop chronic hyperglycemia due to β-cell dysfunction during [...] Read more.
Gestational diabetes mellitus (GDM) is a significant pregnancy complication linked to perinatal complications and an elevated risk of future metabolic disorders for both mothers and their children. GDM is diagnosed when women without prior diabetes develop chronic hyperglycemia due to β-cell dysfunction during gestation. Global research focuses on the association between GDM and single nucleotide polymorphisms (SNPs) and aims to enhance our understanding of GDM’s pathogenesis, predict its risk, and guide patient management. This review offers a summary of various SNPs linked to a heightened risk of GDM and explores their biological mechanisms within the tissues implicated in the development of the condition. Full article
(This article belongs to the Special Issue Molecular Research on Diabetes)
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14 pages, 1649 KiB  
Review
Molecular Mechanisms Linking Diabetes with Increased Risk of Thrombosis
by Lucy Batten, Thozhukat Sathyapalan and Timothy M. Palmer
Int. J. Mol. Sci. 2023, 24(24), 17465; https://doi.org/10.3390/ijms242417465 - 14 Dec 2023
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Abstract
This review will provide an overview of what is currently known about mechanisms linking poor glycaemic control with increased thrombotic risk. The leading causes of death in people with diabetes are strokes and cardiovascular disease. Significant morbidity is associated with an increased risk [...] Read more.
This review will provide an overview of what is currently known about mechanisms linking poor glycaemic control with increased thrombotic risk. The leading causes of death in people with diabetes are strokes and cardiovascular disease. Significant morbidity is associated with an increased risk of thrombosis, resulting in myocardial infarction, ischaemic stroke, and peripheral vascular disease, along with the sequelae of these events, including loss of functional ability, heart failure, and amputations. While the increased platelet activity, pro-coagulability, and endothelial dysfunction directly impact this risk, the molecular mechanisms linking poor glycaemic control with increased thrombotic risk remain unclear. This review highlights the complex mechanisms underlying thrombosis prevalence in individuals with diabetes and hyperglycaemia. Post-translational modifications, such as O-GlcNAcylation, play a crucial role in controlling protein function in diabetes. However, the role of O-GlcNAcylation remains poorly understood due to its intricate regulation and the potential involvement of multiple variables. Further research is needed to determine the precise impact of O-GlcNAcylation on specific disease processes. Full article
(This article belongs to the Special Issue Molecular Research on Diabetes)
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