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Nutr Rev. 2015 Dec;73(12):858-68. doi: 10.1093/nutrit/nuv042. Epub 2015 Oct 22.

Glutathionyl systems and metabolic dysfunction in obesity.

Author information

1
M.J. Picklo and E.E. Vomhof-DeKrey are with the Grand Forks Human Nutrition Research Center, USDA-ARS, Grand Forks, North Dakota, USA. M.J. Picklo is with the Department of Chemistry, University of North Dakota, Grand Forks, North Dakota, USA. E.K. Long is with the Department of Surgery, University of Minnesota, Minneapolis, Minnesota USA. matthew.picklo@ars.usda.gov.
2
M.J. Picklo and E.E. Vomhof-DeKrey are with the Grand Forks Human Nutrition Research Center, USDA-ARS, Grand Forks, North Dakota, USA. M.J. Picklo is with the Department of Chemistry, University of North Dakota, Grand Forks, North Dakota, USA. E.K. Long is with the Department of Surgery, University of Minnesota, Minneapolis, Minnesota USA.

Abstract

Oxidative stress is associated with obesity. However, glutathione (GSH), one of the body's most abundant antioxidants, plays dual and seemingly contradictory roles in the development of obesity and its comorbidities. Glutathione has complex metabolic and biochemical fates and is a cofactor for several enzymes that function in modifying obesity-related responses. For example, depletion of GSH increases energy metabolism and reduces adipose accretion, while elevation of GSH peroxidase activity induces insulin resistance. This review summarizes the literature linking GSH and its related enzymes, GSH peroxidase, glutaredoxins, and glutathione S-transferases, to obesity and its pertinent endpoints (e.g., energy metabolism, inflammation, and insulin resistance).

KEYWORDS:

glutathione; glutathione S-transferase; glutathione peroxidase; glutathionylation; inflammation.; insulin; obesity

PMID:
26493322
DOI:
10.1093/nutrit/nuv042
[Indexed for MEDLINE]

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