Role of Metabolic Factors and Their Interactions on Diabetes and Its Complications

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (31 May 2026) | Viewed by 1799

Editor


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Guest Editor
Chronic Disease Epidemiology Laboratory, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA
Interests: diabetes; obesity; nutrition

Special Issue Information

Dear Colleagues

This Special Issue aims to provide a comprehensive overview of the latest research on how metabolic factors such as obesity, hypertension, dyslipidemia, and insulin resistance contribute to diabetes onset and progression. It will also delve into the interactions between these factors, examining how they synergistically influence the risk and severity of diabetes-related complications, including cardiovascular disease, nephropathy, neuropathy, and retinopathy. A key focus will be on the application of new technologies in bioinformatics, such as machine learning algorithms, multi-omics integration, and advanced data analytics, which are revolutionizing our understanding of the metabolic pathways involved in diabetes. By bringing together cutting-edge studies from diverse fields, this Special Issue seeks to enhance our understanding of the multifactorial nature of diabetes and identify potential avenues for prevention and treatment. Researchers, clinicians, and public health professionals will find valuable insights into the metabolic underpinnings of diabetes and its far-reaching health implications.

Dr. Yun Shen
Guest Editor

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Keywords

  • metabolic risk factors
  • diabetes comorbidities
  • bioinformatics
  • machine learning
  • multi-omics integration
  • cardiovascular disease
  • dyslipidemia
  • insulin resistance
  • biomarkers

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Published Papers (1 paper)

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Research

20 pages, 1940 KB  
Article
Evidence for a Cytokine-Sensitive Network of Iron-Associated Genes That Protects Pancreatic Islets Against Ferroptosis
by Kira G. Slepchenko, Grace P. Counts, Poonam R. Sharma, Si Chen, Kathryn L. Corbin, Farhan M. Qureshi, Robert A. Colvin, C. Martin Lawrence and Craig S. Nunemaker
Metabolites 2026, 16(2), 112; https://doi.org/10.3390/metabo16020112 - 4 Feb 2026
Viewed by 908
Abstract
Background/Objectives: The micronutrient iron is closely connected to inflammation and is among the complex factors contributing to beta-cell failure in diabetes. High levels of dietary iron increase the risk of developing type 2 diabetes, and excessive iron uptake by beta-cells can cause [...] Read more.
Background/Objectives: The micronutrient iron is closely connected to inflammation and is among the complex factors contributing to beta-cell failure in diabetes. High levels of dietary iron increase the risk of developing type 2 diabetes, and excessive iron uptake by beta-cells can cause oxidative stress and inhibit function. Elevated levels of proinflammatory cytokines in obese individuals, such as interleukin (IL)-1beta and IL-6, increase the risk of developing type 2 diabetes, and there is evidence that these low levels of circulating cytokines can lead to islet dysfunction. Methods: In this study, gene microarray and other data were analyzed for expression differences in islets treated for 48 h with 10 pg/mL IL-1beta + 20 pg/mL IL-6 as a model of low-grade inflammation versus untreated. Results: Three iron-associated genes were among the most cytokine-sensitive in the mouse genome: Hamp, Steap4, and Lcn2. These proteins are all involved with increasing/retaining cellular iron. We hypothesized that increased cellular iron would lead to increased susceptibility to ferroptosis. Surprisingly, 24 h pre-exposure to low-grade inflammation, which upregulates this iron-gene network, prevented subsequent erastin-induced ferroptosis. We also found that Steap4 overexpression reduced islet dysfunction caused by high-dose proinflammatory cytokines (10× low-dose), suggesting an overall protective effect. Steap4 overexpression also upregulated Hamp and Lcn2, suggesting Steap4 regulates these cytokine-sensitive iron genes.; in contrast, ferritin and ferroportin gene expression, which are not sensitive to cytokines, were unchanged. Conclusions: These data suggest an inflammation-induced network of genes involved in cellular iron uptake and retention plays a protective role in islets against oxidative stress and ferroptosis. Full article
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