Mitochondrial dysfunction in obesity

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

Research output: Contribution to journalReview article

23 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)26-32
Number of pages7
JournalLife Sciences
Volume192
DOIs
StatePublished - Jan 1 2018
Externally publishedYes

Fingerprint

Oxidative stress
Obesity
Reactive Oxygen Species
Neurology
Oxidative Stress
Tissue
Apoptosis
Electron Transport
Blood-Brain Barrier
Central Nervous System
Nutrients
Citric Acid Cycle
Hypothalamus
Hippocampus
Inflammation
Food

Keywords

  • Apoptosis
  • Inflammation
  • Mitochondrial dysfunction
  • Obesity
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Haas de Mello, A., Costa, A. B., Engel, J. D. G., & Rezin, G. T. (2018). Mitochondrial dysfunction in obesity. Life Sciences, 192, 26-32. https://doi.org/10.1016/j.lfs.2017.11.019

Mitochondrial dysfunction in obesity. / Haas de Mello, Aline; Costa, Ana Beatriz; Engel, Jéssica Della Giustina; Rezin, Gislaine Tezza.

In: Life Sciences, Vol. 192, 01.01.2018, p. 26-32.

Research output: Contribution to journalReview article

Haas de Mello, Aline ; Costa, Ana Beatriz ; Engel, Jéssica Della Giustina ; Rezin, Gislaine Tezza. / Mitochondrial dysfunction in obesity. In: Life Sciences. 2018 ; Vol. 192. pp. 26-32.
@article{01b6cc62642f4d6786a1bb0cbeb4f4aa,
title = "Mitochondrial dysfunction in obesity",
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.",
keywords = "Apoptosis, Inflammation, Mitochondrial dysfunction, Obesity, Oxidative stress",
author = "{Haas de Mello}, Aline and Costa, {Ana Beatriz} and Engel, {J{\'e}ssica Della Giustina} and Rezin, {Gislaine Tezza}",
year = "2018",
month = "1",
day = "1",
doi = "10.1016/j.lfs.2017.11.019",
language = "English (US)",
volume = "192",
pages = "26--32",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Mitochondrial dysfunction in obesity

AU - Haas de Mello, Aline

AU - Costa, Ana Beatriz

AU - Engel, Jéssica Della Giustina

AU - Rezin, Gislaine Tezza

PY - 2018/1/1

Y1 - 2018/1/1

N2 - 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.

AB - 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.

KW - Apoptosis

KW - Inflammation

KW - Mitochondrial dysfunction

KW - Obesity

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=85034566563&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85034566563&partnerID=8YFLogxK

U2 - 10.1016/j.lfs.2017.11.019

DO - 10.1016/j.lfs.2017.11.019

M3 - Review article

VL - 192

SP - 26

EP - 32

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

ER -