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Metabolites
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Mitochondrial Metabolism and Oxidative Stress in Hypertension, Diabetes and Related...
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Mitochondrial Metabolism and Oxidative Stress in Hypertension, Diabetes and Related 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: 30 April 2025 | Viewed by 2512

Special Issue Editor

Prof. Dr. Christian Cortés-Rojo

E-Mail Website
Guest Editor
Instituto de Investigaciones Químico-Biológicas, Universidad Michoacana de San Nicolás de Hidalgo, Morelia, Michoacán, México
Interests: mitochondrial dysfunction in chronic degenerative diseases; functional foods and nutraceuticals in oxidative stress; inflammation and mitochondrial dysfunction in chronic degenerative diseases

Special Issue Information

Dear Colleagues,

Alterations in mitochondrial energy metabolism are one of the underlying causes in the development of diabetes and hypertension and its complications. Mitochondrial dysfunction increases the production of reactive oxygen species (ROS) to deleterious levels and activates various mechanisms that result in tissue damage in both diseases. The dysfunction of mitochondrial energy metabolism in turn negatively alters other processes, further disrupting cellular homeostasis, including mitophagy, autophagy and cell death processes such as apoptosis, necrosis or ferroptosis. This Special Issue is devoted to such topics, including (not exclusively) studies on alterations in the mitochondrial metabolic profile, mitochondrial energy metabolism and mitochondrial oxidative stress in diabetes and hypertension. Topics such as the dysregulation of mitochondrial dynamics (fusion/fission), mitochondrial quality control (mitophagy) and cell death (apoptosis, necrosis, ferroptosis) in diabetes and hypertension are also welcome. The therapeutic use of drugs, nutraceuticals and functional foods for the control of these alterations in diabetes and hypertension is also covered.

Prof. Dr. Christian Cortés-Rojo
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • diabetes
  • hypertension
  • ROS
  • oxidative stress
  • cell death
  • inflammation
  • mitochondrial control quality
  • mitochondrial dynamics
  • mitochondria-targeted molecules
  • nutraceuticals and functional foods

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Published Papers (2 papers)

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Research

19 pages, 3733 KiB  
Article
Evaluation of Unsaponifiable Fraction of Avocado Oil on Liver and Kidney Mitochondrial Function in Rats Fed a High-Fat and High-Carbohydrate Diet
by Marcela González-Montoya, Manuel Alejandro Vargas-Vargas, Olin Torres-Isidro, Claudia Isabel García-Berumen, María Guadalupe Cuiniche-Méndez, Alfredo Saavedra-Molina, Julio Cesar Ontiveros-Rodríguez, Hugo A. García-Gutiérrez, Elizabeth Calderón-Cortés and Christian Cortés-Rojo
Metabolites 2024, 14(8), 431; https://doi.org/10.3390/metabo14080431 - 4 Aug 2024
Viewed by 1184
Abstract
High-fat and high-carbohydrate (HF-HC) diets induce metabolic syndrome via mitochondrial dysfunction and oxidative stress. We have previously shown that this may be prevented by avocado oil, a source of bioactive molecules with antioxidant properties. However, it is unknown if these effects are mediated [...] Read more.
High-fat and high-carbohydrate (HF-HC) diets induce metabolic syndrome via mitochondrial dysfunction and oxidative stress. We have previously shown that this may be prevented by avocado oil, a source of bioactive molecules with antioxidant properties. However, it is unknown if these effects are mediated by the unsaponifiable fraction of avocado oil (UFAO). Thus, we tested if this fraction improves glucose metabolism, bioenergetics and oxidative stress in mitochondria from the kidney and liver of rats fed an HF-HC diet. We found that 12 weeks of an HF-HC diet impaired glucose utilization and increased insulin resistance, which was prevented by UFAO administration. The HF-HC diet decreased respiration, membrane potential and electron transport chain (ETC) function in liver and kidney mitochondria. These mitochondrial dysfunctions were prevented by UFAO intake. Unexpectedly, UFAO increased ROS levels in the mitochondria of control animals and did not decrease them in rats with an HF-HC diet; however, UFAO protects liver and kidney mitochondria from iron-induced oxidative stress. These findings suggest that impairments in glucose metabolism and mitochondrial function by an HF-HC diet may be prevented by UFAO, without decreasing ROS generation but protecting mitochondria from oxidative damage. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Oxidative Stress in Hypertension, Diabetes and Related Complications)
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11 pages, 2062 KiB  
Article
Excess Branched-Chain Amino Acids Suppress Mitochondrial Function and Biogenic Signaling but Not Mitochondrial Dynamics in a Myotube Model of Skeletal Muscle Insulin Resistance
by Lindsey R. VanDerStad, Emily C. Wyatt and Roger A. Vaughan
Metabolites 2024, 14(7), 389; https://doi.org/10.3390/metabo14070389 - 17 Jul 2024
Viewed by 898
Abstract
Branched-chain amino acids (BCAA) are correlated with severity of insulin resistance, which may partially result from mitochondrial dysfunction. Mitochondrial dysfunction is also common during insulin resistance and is regulated in part by altered mitochondrial fusion and fission (mitochondrial dynamics). To assess the effect [...] Read more.
Branched-chain amino acids (BCAA) are correlated with severity of insulin resistance, which may partially result from mitochondrial dysfunction. Mitochondrial dysfunction is also common during insulin resistance and is regulated in part by altered mitochondrial fusion and fission (mitochondrial dynamics). To assess the effect of BCAA on mitochondrial dynamics during insulin resistance, the present study examined the effect of BCAA on mitochondrial function and indicators of mitochondrial dynamics in a myotube model of insulin resistance. C2C12 myotubes were treated with stock DMEM or DMEM with additional BCAA at 0.2 mM, 2 mM, or 20 mM to achieve a continuum of concentrations ranging from physiologically attainable to supraphysiological (BCAA overload) both with and without hyperinsulinemia-mediated insulin resistance. qRT-PCR and Western blot were used to measure gene and protein expression of targets associated with mitochondrial dynamics. Mitochondrial function was assessed by oxygen consumption, and mitochondrial content was measured using mitochondrial-specific staining. Insulin resistance reduced mitochondrial function, peroxisome proliferator-activated receptor gamma coactivator 1-alpha mRNA, and citrate synthase expression mRNA, but not protein expression. Excess BCAA at 20 mM also independently reduced mitochondrial function in insulin-sensitive cells. BCAA did not alter indicators of mitochondrial dynamics at the mRNA or protein level, while insulin resistance reduced mitochondrial fission protein 1 mRNA, but not protein expression. Collectively, BCAA at excessively high levels or coupled with insulin resistances reduce mitochondrial function and content but do not appear to alter mitochondrial dynamics under the tested conditions. Full article
(This article belongs to the Special Issue Mitochondrial Metabolism and Oxidative Stress in Hypertension, Diabetes and Related Complications)
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