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Review
. 2018 Nov 9:15:1-5.
doi: 10.1016/j.jcte.2018.11.001. eCollection 2019 Mar.

Is oxidative stress of adipocytes a cause or a consequence of the metabolic syndrome?

Leonid N Maslov  1 , Natalia V Naryzhnaya  1 , Alla A Boshchenko  1 , Sergey V Popov  1 , Vladimir V Ivanov  2 , Peter R Oeltgen  3
Affiliations
Review

Is oxidative stress of adipocytes a cause or a consequence of the metabolic syndrome?

Leonid N Maslov et al. J Clin Transl Endocrinol. .

Abstract

Metabolic syndrome is accompanied by oxidative stress in animals and humans. The main source of ROS in experimental metabolic syndrome is NADPH oxidase and possibly adipocyte mitochondria. It is now documented that oxidative stress induces insulin resistance of adipocytes and increases secretion of leptin, MCP-1, IL-6, and TNF-α by adipocytes. It was established that oxidative stress induces a decrease in adiponectin production by adipocytes. It has also been shown that obesity itself can induce oxidative stress. Oxidative stress can cause an alteration of intracellular signaling in adipocytes that apparently leads to the formation of insulin resistance of adipocytes. Chronic stress, glucocorticoids, mineralocorticoids, angiotensin-II, TNF-α also play an important role in the pathogenesis of oxidative stress of adipocytes. Oxidative stress is not only a consequence of metabolic syndrome, but also a reason and a foundational link in the pathogenesis of the metabolic syndrome.

Keywords: Adipocytes; Metabolic syndrome; Oxidative stress.

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Figures

Fig. 1
Fig. 1
The relationship of metabolic syndrome and oxidative stress. ROS, reactive oxygen species; SOD, superoxide dismutase; TNF-α, tumor necrosis factor-α.
See this image and copyright information in PMC

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