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Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

ABSTRACT: Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

PROVIDER: PRJNA664402 | ENA |

REPOSITORIES: ENA

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Enterocyte Superoxide Dismutase 2 Deletion Drives Hyperinsulinemia and Obesity

Project description:Compelling evidence support an involvement of oxidative stress and intestinal inflammation as early events in the predisposition and development of obesity and its related comorbidities. Here we show that deficiency of the major mitochondrial antioxidant enzyme superoxide dismutase 2 (SOD2) in the gastrointestinal tract drives spontaneous obesity. Intestinal epithelium-specific Sod2 ablation in mice induced adiposity, inflammation and insulin resistance via phospholipase A2 (PLA2) activation and increased synthesis of omega-6 polyunsaturated fatty acid arachidonic acid. Remarkably, this obese and hyperinsulinemic phenotype was rescued when fed an essential fatty acid deficient diet, which abrogates de novo biosynthesis of arachidonic acid. Data from clinical samples revealed that the negative correlation between intestinal SOD2 mRNA levels and obesity features, such as body mass index and omega-6/omega-3 fatty acid ratio, appears to be conserved between mice and humans. Collectively, our findings suggest a role of intestinal SOD2 levels, PLA2 activity and arachidonic acid in obesity presenting new potential targets of therapeutic interest in the context of this metabolic disorder.

2021-12-31 | GSE158237 | GEO

Enterocyte superoxide dismutase 2 deletion drives obesity.

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Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer

Project description:Reactive oxygen species have been established to play a critical role in pancreatic carcinogenesis. One of the main antioxidant enzymes is mitochondrial superoxide dismutase (Sod2). Sod2 has been shown to affect tumor initiation and metastatic progression in various cancer types. The impact of Sod2 deletion on pancreatic cancer biology and metabolism has so far not been investigated. We therefore generated three individual Sod2 deficient cell lines from murine pancreatic cancer cell lines isolated from KrasG12D mutant mice and analyzed control and knockout lines with RNA-seq.

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Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer

Project description:Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer

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Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

Project description:Superoxide radical anion and other Reactive Oxygen Species are constantly produced during respiration. In mitochondria, the dismutation of the superoxide radical anion is accelerated by the mitochondrial superoxide dismutase 2 (SOD2), an enzyme that has been traditionally associated with antioxidant protection. However, increases in SOD2 expression promote oxidative stress, indicating that there may be a prooxidant role for SOD2. We show that SOD2, which normally binds manganese, can incorporate iron and generate an alternative isoform with peroxidase activity. The switch from manganese to iron allows FeSOD2 to utilize H2O2 to promote oxidative stress. We found that FeSOD2 is formed in cultured cells. FeSOD2 causes mitochondrial dysfunction and higher levels of oxidative stress in cultured cells. We show that formation of FeSOD2 converts an antioxidant defense into a prooxidant peroxidase that leads to cellular changes seen in multiple human diseases.

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Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

Project description:Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

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Fruit derived superoxide dismutase nanozyme for sepsis-induced acute lung injury therapy

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Switch of mitochondrial superoxide dismutase into a prooxidant peroxidase in manganese-deficient cells

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Natural plant-derived superoxide dismutase nanoenzyme for sepsis-induced liver injury therapy.

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Molecular mechanisms of lifespan extension in long-lived mitocondrial superoxide dismutase sod-2 mutants

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