Myeloperoxidase and fat tissue deregulation duringo obesity

DARIO C. RAMIREZ; SANDRA E. GOMEZ-MEJIBA

WASHINGTON DC

Congreso; EXPERIMENTAL BIOLOGY 2011; 2011

FASEB

MYELOPEROXIDASE AND FAT TISSUE DEREGULATION DURING OBESITY DARIO C RAMIREZ and SANDRA E GOMEZ-MEJIBA EXPERIMENTAL THERAPEUTICS, OMRF, OKLAHOMA CITY, OK Macrophages-mediated fat tissue inflammation contributes to low-grade chronic systemic inflammation and insulin resistance (IR) in adipocytes during obesity. However, the agents, targets and mechanistic bases of the oxidation process that occurs in fat during obesity remain unclear. In this study we sought to determine whether myeloperoxidase (MPO) causes inflammation and IR in adipocytes. We used a mouse model of diet-induced obesity and an in vitro model of adipocytes loaded with MPO and stressed with H2O2. The visceral fat of obese mice was infiltrated with macrophages that express MPO, located in crown-like structures in hypoxic areas. Immuno-staining showed MPO also inside the adipocytes, especially around the lipid droplets. Luminol showed that MPO produced HOCl inside adipocytes that was prevented by the MPO inhibitors or resveratrol—a cell permeable scavenger of HOCl. HOCl produced inside the adipocyte caused adipokine deregulation and IR. Immuno-spin trapping with anti-DMPO of adipocytes loaded with MPO and treated with H2O2 and DMPO showed a number of proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. infiltrated with macrophages that express MPO, located in crown-like structures in hypoxic areas. Immuno-staining showed MPO also inside the adipocytes, especially around the lipid droplets. Luminol showed that MPO produced HOCl inside adipocytes that was prevented by the MPO inhibitors or resveratrol—a cell permeable scavenger of HOCl. HOCl produced inside the adipocyte caused adipokine deregulation and IR. Immuno-spin trapping with anti-DMPO of adipocytes loaded with MPO and treated with H2O2 and DMPO showed a number of proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. 2O2. The visceral fat of obese mice was infiltrated with macrophages that express MPO, located in crown-like structures in hypoxic areas. Immuno-staining showed MPO also inside the adipocytes, especially around the lipid droplets. Luminol showed that MPO produced HOCl inside adipocytes that was prevented by the MPO inhibitors or resveratrol—a cell permeable scavenger of HOCl. HOCl produced inside the adipocyte caused adipokine deregulation and IR. Immuno-spin trapping with anti-DMPO of adipocytes loaded with MPO and treated with H2O2 and DMPO showed a number of proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic. 2O2 and DMPO showed a number of proteins targets of oxidation in the adipocyte. Treatments aimed at preventing or stopping MPO-driven oxidation inside adipocytes might offer new therapeutic avenues for preventing obese patients from becoming diabetic.