Troglitazone reduces leptinemia during experimental dexamethasone-induced stress

Background and aims: Recently, we found that profound anorexia observed in a catabolic model induced by chronic glucocorticoid (dexamethasone, Dex) injection could be associated with strong hyperleptinemia. To investigate the implication of leptin in this catabolic stress response, we used a model whereby leptin secretion was inhibited using troglitazone (Trg) concomitantly with a Dex-induced-stress injection. Methods: Adult rats (3 months, n = 12) were stressed with a Dex injection (1.5 mg/kg/day ip, 5 days) and either treated (DXTG(+), n = 6) or not (DXTG(-), n = 6) with Trg (60 mg/kg/day sc, 5 days). These DXTG(+) and DXTG(-) groups were compared with an untreated ad libitum group and a pair-fed group receiving saline ip instead of the Dex injection. The effects of troglitazone treatment on leptin gene expression in adipose tissue, blood glucose, insulin, and on hepatic parameters under stress conditions were determined. Results: Trg treatment specifically diminished leptinemia (30%, DXTG(+) vs DXTG(-), p < 0.05). Insulinemia and glycemia remained unchanged, as did leptin gene expression; food intake improved, but hepatic capacities did not show any alteration. Conclusion: Trg is a useful agent in exploring certain potential effects of leptin on metabolic and immune disorders occurring during aggression.