title: Evaluation of liver glycogen catabolism during hypercortisolism induced by the administration of dexamethasone in rats.
abstract: BACKGROUND
  The contribution of liver glycogen catabolism to hyperglycemia and glucose intolerance induced by pharmacological hypercortisolism were investigated.
  
  
  METHODS
  For this purpose, adult male Wistar rats that received 1.0 mg/kg dexamethasone (DEX) ip at 8:00 a.m. (DEX group) or saline (CON group) once a day for 5 consecutive days were compared.
  
  
  RESULTS
  Experimental hypercortisolism was confirmed by higher (p<0.05) glycemia, lower (p<0.05) body weight and glucose intolerance. In the fed state, the basal glycogen catabolism and the glucagon (1 nM) and epinephrine (2 μM) induced glycogen catabolism were similar between the groups. The activation of glycogen catabolism induced by phenylephrine (2 μM) and isoproterenol (20 μM) were increased (p<0.05) and decreased (p<0.05), respectively, in DEX rats. Furthermore, DEX rats exhibited higher (p<0.05) glycogen catabolism during the infusion of cAMP (3 μM). However, during the infusion of cAMP (15 μM), 6MB-cAMP (3 μM) or cyanide (0.5 mM), the intensification of glycogen breakdown was similar. Thus, in general, hypercortisolism does not influence the basal glycogen catabolism and the liver responsiveness to glycogenolytic agents in the fed state. In contrast with fed state, fasted rats (DEX group) showed a more intense (p<0.05) basal glycogen catabolism.
  
  
  CONCLUSIONS
  The contribution of glycogen catabolism to hyperglycemia during hypercortisolism depends of the nutritional status, starting from a negligible participation in the fed state up to a significant contribution in the fasted state.
authors.affiliation: Department of Pharmacology and Therapeutic, State University of Maringá, Maringá, PR, 87020-900, Brazil.
authors.forename: Thauany M
authors.initials: TM
authors.lastname: Tavoni
authors.forename: Simoni
authors.initials: S
authors.lastname: Obici
authors.forename: Any
authors.initials: A
authors.lastname: de Castro R Marques
authors.forename: Vania C
authors.initials: VC
authors.lastname: Minguetti-Câmara
authors.forename: Rui
authors.initials: R
authors.lastname: Curi
authors.forename: Roberto B
authors.initials: RB
authors.lastname: Bazotte
mesh_terms: D000818:Animals; D001835:Body Weight; D003480:Cushing Syndrome / Q000139:chemically induced* / Q000503:physiopathology; D000242:Cyclic AMP / Q000008:administration & dosage; D003907:Dexamethasone / Q000008:administration & dosage / Q000633:toxicity*; D004837:Epinephrine / Q000008:administration & dosage; D005215:Fasting; D005934:Glucagon / Q000008:administration & dosage; D018149:Glucose Intolerance; D006003:Glycogen / Q000378:metabolism*; D006943:Hyperglycemia / Q000139:chemically induced / Q000503:physiopathology; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar
chemical_list: D003907:Dexamethasone; D006003:Glycogen; D005934:Glucagon; D000242:Cyclic AMP; D004837:Epinephrine