P 110 - Glutathione deprivation improves oxidative capacity but disrupts endocrine role of white adipose tissue in overall metabolic homeostasis

Abstract

Clarification of molecular mechanisms underlying lipid buffering capacity of white adipose tissue (WAT) may aid in the improvement of therapeutic options for obesity and diabetes prevention. Results of our studies have shown that cold-induced regression of WAT involves transient increase of tissue lipid oxidation, uncoupling capacity, an occurrence of browning allsynchronized with increase in adiponectin and resistin synthesis and profound glutathione (GSH) depletion. This GSH decrease prompted us to examine if a decrement of GSH a priori recapitulates cold-induced favorable phenotype of WAT. To this end, room-temperature and cold-exposed rats were treated with L-buthionine-S,R-sulfoximine (BSO). Indeed, BSO treatment reduced rat body weight and lipid content in fat tissue on account of increased OXPHOS and uncoupling capacity of WAT in both, cold-exposed and room-temperature maintained rats. However, in comparison to control, BSO decreased expressions of adiponectin and resistin at room temperature and attenuated their adaptive increase on cold exposure. Decrement of GSH raise lipid burning phenotype in WAT, but it may interfere with endocrine role of WAT in overall metabolic homeostasis maintenance.