Adipose oxidative stress and protein carbonylation

Amy K. Hauck, Yimao Huang, Ann V. Hertzel, David A. Bernlohr

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

Increased oxidative stress and abundance of reactive oxygen species (ROS) are positively correlated with a variety of patho-physiologies, including cardiovascular disease, type 2 diabetes, Alzheimer's disease, and neuroinflammation. In adipose biology, diabetic obesity is correlated with increased ROS in an age- and depot-specific manner and is mechanistically linked to mitochondrial dysfunction, endoplasmic reticulum (ER) stress, potentiated lipolysis, and insulin resistance. The cellular quality control systems that homeostatically regulate oxidative stress in the lean state are down-regulated in obesity as a consequence of inflammatory cytokine pressure leading to the accumulation of oxidized biomolecules. New findings have linked protein, DNA, and lipid oxidation at the biochemical level, and the structures and potential functions of protein adducts such as carbonylation that accumulate in stressed cells have been characterized. The sum total of such regulation and biochemical changes results in alteration of cellular metabolism and function in the obese state relative to the lean state and underlies metabolic disease progression. In this review, we discuss the molecular mechanisms and events underlying these processes and their implications for human health and disease.

Original languageEnglish (US)
Pages (from-to)1083-1088
Number of pages6
JournalJournal of Biological Chemistry
Volume294
Issue number4
DOIs
StatePublished - Jan 25 2019

PubMed: MeSH publication types

  • Journal Article
  • Research Support, N.I.H., Extramural
  • Review

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