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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.

Project description: Not available

| S-EPMC8753186 | biostudies-literature

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.

2025-12-23 | E-MTAB-16320 | biostudies-arrayexpress

Mitochondrial superoxide dismutase controls metabolic plasticity in pancreatic cancer

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

| PRJEB104508 | ENA

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.

2017-12-05 | GSE106206 | GEO

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

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

| PRJNA1173153 | ENA

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.

| PRJNA1169014 | ENA

Superoxide dismutase shapes manganese stoichiometry in Southern Ocean diatoms

Project description:Elemental stoichiometry of biomass is a focal point that connects different biogeochemical cycles. Yet, the mechanistic underpinnings of elemental stoichiometry are poorly quantified in many cases. We combined targeted and untargeted metaproteomics, Bayesian statistical modelling, and geochemical measurements to quantify the contribution of specific proteins to metal stoichiometry in natural populations of Southern Ocean diatoms. Our analyses indicate that a substantial amount of non-photosynthetic manganese (Mn) in diatoms in an Antarctic polynya can be attributed to superoxide dismutases (~0.7 mol Mn : mol Carbon; ~20% of the total cellular Mn quota). We then used cultures and proteomic profiling of the key polar diatom Fragilariopsis cylindrus to identify environmental controls on superoxide dismutases, and discovered that iron concentration has little influence on the abundance of two Mn superoxide dismutases, while Mn limitation induces the depletion of these Mn superoxide dismutases and an accompanying increase of nickel superoxide dismutase. Overall, we combined metaproteomic approaches to quantify proteomic composition and connected these measurements to metal-to-carbon ratios and their responses to metal availability. Because metal quotas are key parameters in some biogeochemical models, our approach provides a direct mechanism for informing ecosystem-scale models with molecular measurements.

2026-08-13 | PXD076644 | Pride

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

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

| PRJNA415919 | ENA

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

Project description:Sepsis-induced liver injury is an important cause of septicemia deaths, this injury is characterized by an overproduction of reactive oxygen species (ROS) within the liver, which activates the inflammatory response and results in the release of numerous inflammatory factors, ultimately leading to liver damage. Thus, the development of medicines capable of eliminating ROS and reducing inflammatory factors holds significant prospects. In this study, we synthesized and characterized a natural superoxide dismutase-mimicking carbon dots (G-CDs) form a greenery Glycyrrhiza with distinctive ROS scavenging ability for SILI therapy. The abundant surface unsaturated groups especially oxhydry and carbonyl groups enable G-CDs to exhibit excellent SOD-like enzyme activity exceeding 10000 U/mg and significantly reduce the excessive production of ROS and inflammatory factors. In addition, G-CDs reduced inflammation, oxidative damage, and tissue damage in the liver of lipopolysaccharide (LPS) induced SILI mice model. Mechanistically, G-CDs protect liver tissue by activating Keap-1/Nrf-2 mediated antioxidant signaling and inhibiting NF-κB-dependent inflammatory responses. In conclusion, this study establishes the potential of G-CDs as a promising therapeutic agent for the treatment SILI.

2025-09-11 | GSE278841 | GEO

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