NADPH oxidases in healthy white adipose tissue and in obesity: function, regulation, and clinical implications

Reactive oxygen species, when produced in a controlled manner, are physiological modulators of healthy white adipose tissue (WAT) expansion and metabolic function. By contrast, unbridled production of oxidants is associated with pathological WAT expansion and the establishment of metabolic dysfuncti...

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Bibliographic Details
Published in:Obesity (Silver Spring, Md.) Md.), 2024-10, Vol.32 (10), p.1799-1811
Main Authors: Jornayvaz, François R., Gariani, Karim, Somm, Emmanuel, Jaquet, Vincent, Bouzakri, Karim, Szanto, Ildiko
Format: Article
Language:English
Subjects:
Adipocytes
Adipocytes - metabolism
Adipose Tissue, White - metabolism
Animals
Antioxidants
Body fat
Diabetes
Diabetes Mellitus, Type 2 - metabolism
Enzymes
Fibroblasts
Gene expression
Homeostasis
Humans
Insulin Resistance
Kinases
Metabolism
Mice
Mitochondria
NADPH Oxidases - metabolism
Obesity
Obesity - metabolism
Oxidation
Oxidation-Reduction
Physiology
Proteins
Reactive oxygen species
Reactive Oxygen Species - metabolism
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Summary:Reactive oxygen species, when produced in a controlled manner, are physiological modulators of healthy white adipose tissue (WAT) expansion and metabolic function. By contrast, unbridled production of oxidants is associated with pathological WAT expansion and the establishment of metabolic dysfunctions, most notably insulin resistance and type 2 diabetes mellitus. NADPH oxidases (NOXs) produce oxidants in an orderly fashion and are present in adipocytes and in other diverse WAT‐constituent cell types. Recent studies have established several links between aberrant NOX‐derived oxidant production, adiposity, and metabolic homeostasis. The objective of this review is to highlight the physiological roles attributed to diverse NOX isoforms in healthy WAT and summarize current knowledge of the metabolic consequences related to perturbations in their adequate oxidant production. We detail WAT‐related alterations in preclinical investigations conducted in NOX‐deficient murine models. In addition, we review clinical studies that have employed NOX inhibitors and currently available data related to human NOX mutations in metabolic disturbances. Future investigations aimed at understanding the integration of NOX‐derived oxidants in the regulation of the WAT cellular redox network are essential for designing successful redox‐related precision therapies to curb obesity and attenuate obesity‐associated metabolic pathologies.
ISSN:1930-7381
1930-739X
1930-739X
DOI:10.1002/oby.24113