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Molecular Insights into Type 2 Diabetes and Its Complications

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 January 2025 | Viewed by 3403

Special Issue Editor


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Guest Editor
Department of Medical and Surgical Sciences, University Magna Græcia, 88100 Catanzaro, Italy
Interests: obesity; type-2 diabetes; metabolic syndrome; endothelial dysfunction; hypertension; target organ damage
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Special Issue Information

Dear Colleagues,

Type 2 diabetes is on the rise and has become a widespread epidemic in recent years. It is one of the leading causes of cardiovascular disease, blindness, end-stage renal disease, and non­traumatic lower-limb amputations, leading to growing social and clinical burdens globally. As a result, an enriched understanding of the pathogenesis of type 2 diabetes along with attempts to sort out and carry out effective approaches to prevent or treat type 2 diabetes or its macro- and micro-vascular complications are of paramount importance.

A large body of evidence has well documented that metabolic defects, such as islet β-cell dysfunction, reduced incretin response, and impaired autonomic function, are commonly observed in patients with type 2 diabetes. They may drive the development of type 2 diabetes and contribute to the increased risk of diabetes-related complications. The aim of this Special Issue is to promote the latest research in physiology that focuses on the metabolic defects underlying the onset of type 2 diabetes or its complications, with a particular focus on the association between type 2 diabetes mellitus and cardiovascular disease, with direct or indirect connections to the clinical applications and/or practices. We also plan to advance our knowledge about the effectiveness of lifestyle modifications, such as increased physical activity or reduced sedentary time, for managing type 2 diabetes. We will focus on the mechanisms that mediate alterations of metabolic defects induced by lifestyle modifications, wishing to provide interactions and/or communications between basic and clinical researchers. Manuscripts in the form of original articles, reviews, and commentaries are welcome for submission to this Special Issue.

Prof. Dr. Maria Perticone
Guest Editor

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Keywords

  • diabetes
  • metabolic defects
  • β-cell function
  • dietary intervention
  • physical exercise

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Published Papers (1 paper)

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Research

17 pages, 3810 KiB  
Article
Pyridoxamine Alleviates Cardiac Fibrosis and Oxidative Stress in Western Diet-Induced Prediabetic Rats
by Sarah D’Haese, Lisa Claes, Eva Jaeken, Dorien Deluyker, Lize Evens, Ellen Heeren, Sibren Haesen, Lotte Vastmans, Ivo Lambrichts, Kristiaan Wouters, Casper G. Schalkwijk, Dominique Hansen, BO Eijnde and Virginie Bito
Int. J. Mol. Sci. 2024, 25(15), 8508; https://doi.org/10.3390/ijms25158508 - 4 Aug 2024
Cited by 1 | Viewed by 2942
Abstract
Individuals with type 2 diabetes mellitus (T2DM) are at an increased risk for heart failure, yet preventive cardiac care is suboptimal in this population. Pyridoxamine (PM), a vitamin B6 analog, has been shown to exert protective effects in metabolic and cardiovascular diseases. [...] Read more.
Individuals with type 2 diabetes mellitus (T2DM) are at an increased risk for heart failure, yet preventive cardiac care is suboptimal in this population. Pyridoxamine (PM), a vitamin B6 analog, has been shown to exert protective effects in metabolic and cardiovascular diseases. In this study, we aimed to investigate whether PM limits adverse cardiac remodeling and dysfunction in rats who develop T2DM. Male rats received a standard chow diet or Western diet (WD) for 18 weeks to induce prediabetes. One WD group received additional PM (1 g/L) via drinking water. Glucose tolerance was assessed with a 1 h oral glucose tolerance test. Cardiac function was evaluated using echocardiography and hemodynamic measurements. Histology on left ventricular (LV) tissue was performed. Treatment with PM prevented the increase in fasting plasma glucose levels compared to WD-fed rats (p < 0.05). LV cardiac dilation tended to be prevented using PM supplementation. In LV tissue, PM limited an increase in interstitial collagen deposition (p < 0.05) seen in WD-fed rats. PM tended to decrease 3-nitrotyrosine and significantly lowered 4-hydroxynonenal content compared to WD-fed rats. We conclude that PM alleviates interstitial fibrosis and oxidative stress in the hearts of WD-induced prediabetic rats. Full article
(This article belongs to the Special Issue Molecular Insights into Type 2 Diabetes and Its Complications)
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