06 / Involvement of microsomal prostaglandin E synthase-1 (mPGES-1) in diet-induced adiposity
Obesity is a disease characterized by an excess of nutrients, which, in the long term, leads to major health problems. Obesity is associated with a chronic low grade inflammation at central structures and peripheral organs. Among the affected organs, the inflammation of adipose tissues seems to play a key role in the development of this disease. The prostaglandin E2 (PGE2) is a well-known mediator of inflammation whose expression is dysregulated over obesity. The final step of PGE2 synthesis is catalyzed by several prostaglandin E synthases (PGES), but only the microsomal PGES-1 (mPGES-1) is inducible under inflammatory conditions. Although PGE2 appears as a potential mediator linking obesity and inflammation, few studies have investigated the role of mPGES-1 in obesity. In this context, we showed that mPGES-1 expression is significantly decreased in adipose tissue and liver of obese mice. Then, we observed that mice deleted for the mPGES-1 enzyme (mPGES-1-/- mice) were resistant to diet-induced adiposity. They exhibited a significant decrease in body weight gain and adiposity, compared with control mice fed with the same fat-diet. Interestingly, mPGES-1-/- mice also displayed a reduced inflammation of white adipose tissue. Altogether, these results showed that mPGES-1 inhibition contributes to decrease inflammation linked to obesity, and constitutes a potential target for obesity and comorbidities treatment.