Enterocyte superoxide dismutase 2 deletion drives obesity

Oihane Garcia-Irigoyen, Fabiola Bovenga, Marilidia Piglionica, Elena Piccinin, Marica Cariello, Maria Arconzo, Claudia Peres, Paola Antonia Corsetto, Angela Maria Rizzo, Marta Ballanti, Rossella Menghini, Geltrude Mingrone, Philippe Lefebvre, Bart Staels, Takuji Shirasawa, Carlo Sabbà, Gaetano Villani, Gianfrancesco Maria Villani, Massimo Federici, Marco FedericiAntonio Moschetta

Risultato della ricerca: Contributo in rivistaArticolo in rivista


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 and inflammation via phospholipase A2 (PLA2) activation and increased release of omega-6 polyunsaturated fatty acid arachidonic acid. Remarkably, this obese 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 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.
Lingua originaleEnglish
pagine (da-a)N/A-N/A
Stato di pubblicazionePubblicato - 2022


  • Lipid
  • Molecular physiology
  • Obesity medicine


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