title: Troglitazone reduces leptinemia during experimental dexamethasone-induced stress.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  Trg is a useful agent in exploring certain potential effects of leptin on metabolic and immune disorders occurring during aggression.
authors.affiliation: Laboratoire de Biochimie, Biologie Moléculaire et Nutrition, EA2416, Faculté de Pharmacie, Clermont-Ferrand, France. Florence.Caldefie-Chezet@u-clermont1.fr
authors.forename: F
authors.initials: F
authors.lastname: Caldefie-Chézet
authors.forename: A
authors.initials: A
authors.lastname: Poulin
authors.forename: A
authors.initials: A
authors.lastname: Enreille-Leger
authors.forename: M-P
authors.initials: MP
authors.lastname: Vasson
mesh_terms: D017667:Adipocytes / Q000502:physiology; D000273:Adipose Tissue / Q000166:cytology / Q000502:physiology; D000818:Animals; D000855:Anorexia / Q000139:chemically induced / Q000378:metabolism / Q000503:physiopathology; D001786:Blood Glucose / Q000187:drug effects; D001835:Body Weight; D056486:Chemical and Drug Induced Liver Injury / Q000503:physiopathology; D002839:Chromans / Q000494:pharmacology*; D003907:Dexamethasone / Q000633:toxicity*; D004195:Disease Models, Animal; D004435:Eating; D005938:Glucocorticoids / Q000633:toxicity*; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood* / Q000235:genetics; D008297:Male; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013312:Stress, Physiological / Q000139:chemically induced / Q000378:metabolism* / Q000503:physiopathology; D045162:Thiazolidinediones / Q000494:pharmacology*; D000077288:Troglitazone
chemical_list: D001786:Blood Glucose; D002839:Chromans; D005938:Glucocorticoids; D007004:Hypoglycemic Agents; D007328:Insulin; D020738:Leptin; D012333:RNA, Messenger; D045162:Thiazolidinediones; D003907:Dexamethasone; D000077288:Troglitazone