Mitochondrial dysfunction in obesity

de Mello, Aline Haas; Costa, Ana Beatriz; Engel, Jéssica Della Giustina; Rezin, Gislaine Tezza

doi:10.1016/j.lfs.2017.11.019

Cited by 508Mitochondrial Function and PathologyAutophagy in Disease and TherapyAdipose Tissue and Metabolism

Mitochondrial dysfunction in obesity

de Mello, Aline Haas, Costa, Ana Beatriz, Engel, Jéssica Della Giustina, Rezin, Gislaine Tezza·2018·Life Sciences

DOI 10.1016/j.lfs.2017.11.019

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Abstract

Obesity leads to various changes in the body. Among them, the existing inflammatory process may lead to an increase in the production of reactive oxygen species (ROS) and cause oxidative stress. Oxidative stress, in turn, can trigger mitochondrial changes, which is called mitochondrial dysfunction. Moreover, excess nutrients supply (as it commonly is the case with obesity) can overwhelm the Krebs cycle and the mitochondrial respiratory chain, causing a mitochondrial dysfunction, and lead to a higher ROS formation. This increase in ROS production by the respiratory chain may also cause oxidative stress, which may exacerbate the inflammatory process in obesity. All these intracellular changes can lead to cellular apoptosis. These processes have been described in obesity as occurring mainly in peripheral tissues. However, some studies have already shown that obesity is also associated with changes in the central nervous system (CNS), with alterations in the blood-brain barrier (BBB) and in cerebral structures such as hypothalamus and hippocampus. In this sense, this review presents a general view about mitochondrial dysfunction in obesity, including related alterations, such as inflammation, oxidative stress, and apoptosis, and focusing on the whole organism, covering alterations in peripheral tissues, BBB, and CNS.

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Skeletal muscle experiences elevated ROS production due to cellular responses to elevated free fatty acids and hyperglycemia in obesity.
“Notably, skeletal muscle experiences an elevated ROS production due to cellular responses to elevated levels of free fatty acids and hyperglycemia in obesity [18, 19].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [19]
Dysregulated mitophagy can impact mitochondrial quantity and function.
“Dysregulated mitophagy, however, can impact the mitochondrial quantity and function [19].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [19]
Mitochondrial dysfunction in obesity leads to decreased mitochondrial content, decreased genetic material, and decreased rate of OXPHOS.
“Ultimately, this dysfunction leads to decreased mitochondrial content, decreased genetic material, and decreased rate of OXPHOS [19, 20].”
From Mitochondrial Adaptation in Skeletal Muscle: Impact of Obesity, Caloric Restriction, and Dietary Compounds (2024) · cites this paper as [19]
Oxidative stress is usually observed in adipocytes during obesity.
“Oxidative stress is usually observed in adipocytes during obesity.”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [230]
During obesity, excessive accumulation of triglycerides in adipocytes leads to cellular and organelle dysfunction.
“Indeed, during obesity, excessive accumulation of triglycerides in adipocytes leads to cellular and organelle dysfunction [230,231].”
From Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases (2019) · cites this paper as [230]

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Authors: de Mello, A. H., Costa, A. B., Engel, J. D. G., & Rezin, G. T.
Affiliations: Universidade do Sul de Santa Catarina (BR)
ORCID: Costa, Ana Beatriz
Rezin, Gislaine Tezza
Venue: Life Sciences
Publisher: Elsevier BV
Published: 2018-01
Volume: 192
Pages: 26-32
ISSN: 0024-3205 (ISSN-L)
DOI: 10.1016/j.lfs.2017.11.019
OpenAlex: W2770053197
Cited by: 508
References: 97
Citations by year: 2026: 56 · 2025: 85 · 2024: 89 · 2023: 78 · 2022: 64 · 2021: 50 · 2020: 47 · 2019: 29 · 2018: 10
FWCI: 2.20
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Life Sciences (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
Keywords: mitochondrial dysfunction, obesity, oxidative stress, reactive oxygen species, inflammation, apoptosis, TCA cycle, mitochondrial respiratory chain, blood-brain barrier, hypothalamus, hippocampus, central nervous system, peripheral tissues
MeSH terms: Animals, Blood-Brain Barrier, Humans, Inflammation, Mitochondria, Obesity, Oxidative Stress, Mitochondrial Diseases

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