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Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases, 3rd Edition

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 (31 October 2024) | Viewed by 2434

Special Issue Editors


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Guest Editor
Department for Life Quality Studies, Alma Mater Studiorum, University of Bologna, Bologna, Italy
Interests: nutritional biochemistry; neurodegenerative diseases; oxidative stress; inflammation; nutraceuticals; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The great increase in life expectancy is linked to the necessity of counteracting chronic degenerative diseases, e.g., cancer, metabolic syndrome, type 2 diabetes, and cardiovascular as well as neurodegenerative diseases that affect a high percentage of the population, since oxidative stress and inflammation are common features of these diseases and impact the functions and structures of organs and tissues differently.

As volumes one and two of the Special Issues “Strategies to Counteract Oxidative Stress and Inflammation in Chronic-Degenerative Diseases” have been successful, we will be exploring this issue further in the International Journal of Molecular Sciences (ISSN: 1422-0067, IF: 5.600, and JCR Category Q1). In this third Special Issue, we collect original articles and reviews on this multifaceted topic that still remains largely unexplored, in order to provide support for the development of novel potential therapeutic approaches.

Suggested topics include, but are not limited to, the following:

  • Cellular and molecular mechanisms to counteract oxidative stress and inflammation in aging and chronic diseases;
  • Dietetic strategies for the prevention of chronic diseases;
  • Oxidative stress as a target for interventions;
  • Association of drugs with antioxidant or anti-inflammatory compounds for the therapy of chronic diseases.

Related papers can be found at the following links:

https://www.mdpi.com/journal/ijms/special_issues/chronic_degenerative_diseases.

https://www.mdpi.com/journal/ijms/special_issues/Chronic_Degenerative_Diseases_II.

Dr. Cecilia Prata
Dr. Cristina Angeloni
Dr. Tullia Maraldi
Guest Editors

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Keywords

  • chronic-degenerative diseases
  • oxidative stress
  • inflammation
  • nutrition
  • nutraceuticals
  • stem cell therapy

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Published Papers (1 paper)

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Research

24 pages, 3534 KiB  
Article
Environmental Enrichment Prevents Gut Dysbiosis Progression and Enhances Glucose Metabolism in High-Fat Diet-Induced Obese Mice
by Rubiceli Manzo, Luigui Gallardo-Becerra, Sol Díaz de León-Guerrero, Tomas Villaseñor, Fernanda Cornejo-Granados, Jonathan Salazar-León, Adrian Ochoa-Leyva, Gustavo Pedraza-Alva and Leonor Pérez-Martínez
Int. J. Mol. Sci. 2024, 25(13), 6904; https://doi.org/10.3390/ijms25136904 - 24 Jun 2024
Viewed by 1998
Abstract
Obesity is a global health concern implicated in numerous chronic degenerative diseases, including type 2 diabetes, dyslipidemia, and neurodegenerative disorders. It is characterized by chronic low-grade inflammation, gut microbiota dysbiosis, insulin resistance, glucose intolerance, and lipid metabolism disturbances. Here, we investigated the therapeutic [...] Read more.
Obesity is a global health concern implicated in numerous chronic degenerative diseases, including type 2 diabetes, dyslipidemia, and neurodegenerative disorders. It is characterized by chronic low-grade inflammation, gut microbiota dysbiosis, insulin resistance, glucose intolerance, and lipid metabolism disturbances. Here, we investigated the therapeutic potential of environmental enrichment (EE) to prevent the progression of gut dysbiosis in mice with high-fat diet (HFD)-induced metabolic syndrome. C57BL/6 male mice with obesity and metabolic syndrome, continuously fed with an HFD, were exposed to EE. We analyzed the gut microbiota of the mice by sequencing the 16s rRNA gene at different intervals, including on day 0 and 12 and 24 weeks after EE exposure. Fasting glucose levels, glucose tolerance, insulin resistance, food intake, weight gain, lipid profile, hepatic steatosis, and inflammatory mediators were evaluated in serum, adipose tissue, and the colon. We demonstrate that EE intervention prevents the progression of HFD-induced dysbiosis, reducing taxa associated with metabolic syndrome (Tepidimicrobium, Acidaminobacteraceae, and Fusibacter) while promoting those linked to healthy physiology (Syntrophococcus sucrumutans, Dehalobacterium, Prevotella, and Butyricimonas). Furthermore, EE enhances intestinal barrier integrity, increases mucin-producing goblet cell population, and upregulates Muc2 expression in the colon. These alterations correlate with reduced systemic lipopolysaccharide levels and attenuated colon inflammation, resulting in normalized glucose metabolism, diminished adipose tissue inflammation, reduced liver steatosis, improved lipid profiles, and a significant reduction in body weight gain despite mice’s continued HFD consumption. Our findings highlight EE as a promising anti-inflammatory strategy for managing obesity-related metabolic dysregulation and suggest its potential in developing probiotics targeting EE-modulated microbial taxa. Full article
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