Mitochondrial dysfunction in obesity

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

Research output: Contribution to journalReview articlepeer-review

65 Scopus citations

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

Keywords

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

ASJC Scopus subject areas

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

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