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Dietary Components, Oxidative Stress and Metabolic Diseases

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrition and Metabolism".

Deadline for manuscript submissions: 25 September 2025 | Viewed by 526

Special Issue Editors


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Guest Editor
Department of Pharmaceutical Sciences, University of Perugia, 06123 Perugia, Italy
Interests: metabolism; foods; oxidative stress; inflammation; metabolic diseases
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Biology, University of Naples Federico II, 80126 Naples, Italy
Interests: nutrition; inflammation; oxidative stress; metabolic diseases, mitochondria function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Nutrition plays a crucial role in the prevention of chronic diseases, as most of them can be related to lifestyle factors. In particular, foods can affect cellular oxidative stress, which is a risk factor for various diseases. Oxidative stress is caused by an imbalance between the amount of reactive oxygen species and the body’s antioxidant capacity. In this oxidant/antioxidant balance, the diet plays a crucial role. Indeed, dietary nutrients can influence individuals’ total antioxidant capacity, modulating the degree of oxidative stress and affecting the incidence of diseases related to oxidation. Food components can impair the balance between antioxidant and pro-oxidant agents, causing metabolic alterations. The goal of this Special Issue is to assemble a collection of original research and review articles describing the role of foods as a link between cellular oxidative stress and metabolic diseases. Manuscripts that investigate regulatory mechanisms and pathologies related to oxidative stress, focused on the critical role of foods or nutritional interventions, will be considered.

Dr. Gina Cavaliere
Dr. Giovanna Trinchese
Dr. Fabiano Cimmino
Guest Editors

Manuscript Submission Information

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Keywords

  • nutrition
  • metabolism
  • diet
  • foods
  • oxidative stress
  • antioxidant
  • metabolic diseases

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Published Papers (1 paper)

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Research

15 pages, 1754 KiB  
Article
Maternal Nutritional Programming: Sex-Specific Cardiovascular and Immune Outcomes Following Perinatal High-Fat Diet Exposure
by Yasir Alsiraj, Hong Huang, Robin Shoemaker, Brandon Schanbacher, Margaret Murphy, Peter Giannone and John A. Bauer
Nutrients 2025, 17(9), 1464; https://doi.org/10.3390/nu17091464 - 26 Apr 2025
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Abstract
Background: The long-term effects of a perinatal high-fat diet on the cardiovascular function of offspring are not well elucidated. We hypothesize that perinatal exposure to a high-fat diet alters adult cardiovascular and immune responses in a sex-specific manner. Methods: Male and female offspring [...] Read more.
Background: The long-term effects of a perinatal high-fat diet on the cardiovascular function of offspring are not well elucidated. We hypothesize that perinatal exposure to a high-fat diet alters adult cardiovascular and immune responses in a sex-specific manner. Methods: Male and female offspring were born to perinatal high-fat (pHFD) or control diet (pCD)-fed C57BL/6 mothers and weaned to a control diet. Cardiovascular function (baseline and response to an acute isoproterenol stress test) was quantified at 8 weeks of age, and acute blood inflammatory response to a single low dose of lipopolysaccharide at 9 weeks of age. Results: Male pHFD offspring had identical baseline cardiovascular function compared to pCD mice but a blunted response to isoproterenol (20–45% reductions in cardiac output, stroke volume, and left ventricular fractional shortening). In contrast, baseline cardiovascular parameters were reduced in female pHFD compared to pCD offspring, but there was no effect of perinatal diet on response to isoproterenol. Concentrations of TNF-α and IL-6 in plasma two hours after a low-dose LPS administration were highest in female pCD mice. Conclusions: Perinatal high-fat diet exposure resulted in sex-specific adaptations in cardiovascular function and immune response. Female offspring displayed baseline impairments, whereas male offspring showed latent vulnerability under stress. These differences may reflect underlying hormonal or epigenetic mechanisms that diverge by sex. Future studies should examine the roles of sex hormones and gene regulation pathways to better understand these dimorphic outcomes. These findings emphasize the importance of maternal diet in shaping offspring cardiometabolic risks and highlight potential avenues for nutritional interventions during pregnancy. Full article
(This article belongs to the Special Issue Dietary Components, Oxidative Stress and Metabolic Diseases)
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