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- W2891650407 abstract "In the United States, obesity is a major health problem that negatively impacts life quality and expectancy. In obesity increased levels of reactive oxygen species, increased levels of inflammatory cytokines, and altered iron homeostasis occur, however the mechanisms involved are unresolved. Heme oxygenase (HO-1) confers cytoprotection against oxidative stress and, through its activity, liberates iron from heme, upregulating ferritin, responsible for sequestering free iron. We examined the effect of the HO-1 inducer, cobalt protoporphyrin (CoPP), on the regulation of iron homeostasis in liver of obese mice. In obese mice HO-1 expression was lower (p < 0.05) and cytokine levels higher (p< 0.05) compared to age matched lean mice. HO-1 induction lowered body weight, serum levels of TNF-α and IL-6 (p< 0.05) and cellular levels of iron. In particular, CoPP increased ferritin levels and icreased levels of ferroportin and decreased IREB1 and hepcidin (p< 0.05). Conversely, inhibition of HO activity reversed all of these beneficial effects. The decrease in oxidative stress, via HO-1 induction and increased HO-1 activity, was associated with decreased cellular iron overload. These findings point to an effective strategy in the treatment of the metabolic consequences of obesity through alteration of liver iron homeostasis." @default.
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- W2891650407 date "2011-04-01" @default.
- W2891650407 modified "2023-10-09" @default.
- W2891650407 title "HO‐1 Involvement In Iron Homeostasis In Liver Of Obese Mice" @default.
- W2891650407 doi "https://doi.org/10.1096/fasebj.25.1_supplement.661.7" @default.
- W2891650407 hasPublicationYear "2011" @default.
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