Evaluation of liver glycogen catabolism during hypercortisolism induced by the administration of dexamethasone in rats

The contribution of liver glycogen catabolism to hyperglycemia and glucose intolerance induced by pharmacological hypercortisolism were investigated. For this purpose, adult maleWistar rats that received 1.0mg/kg dexamethasone (DEX) ip at 8:00 a.m. (DEX group) or saline (CON group) once a day for 5...

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Bibliographic Details
Published in:Pharmacological reports 2013-01, Vol.65 (1), p.144-151
Main Authors: Tavoni, Thauany M., Obici, Simoni, R. Marques, Any de Castro, Minguetti-Câmara, Vania C., Curi, Rui, Bazotte, Roberto B.
Format: Article
Language:English
Subjects:
Animals
Body Weight
cAMP
Cushing Syndrome - chemically induced
Cushing Syndrome - physiopathology
Cyclic AMP - administration & dosage
dexamethasone
Dexamethasone - administration & dosage
Dexamethasone - toxicity
Drug Safety and Pharmacovigilance
Epinephrine - administration & dosage
Fasting
Glucagon - administration & dosage
Glucose Intolerance
glucose tolerance
Glycogen - metabolism
glycogenolysis
glycolysis
hypercortisolis
hyperglycemia
Hyperglycemia - chemically induced
Hyperglycemia - physiopathology
insulin resistance
Liver - drug effects
Liver - metabolism
Male
Pharmacotherapy
Pharmacy
Rats
Rats, Wistar
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Summary:The contribution of liver glycogen catabolism to hyperglycemia and glucose intolerance induced by pharmacological hypercortisolism were investigated. For this purpose, adult maleWistar rats that received 1.0mg/kg dexamethasone (DEX) ip at 8:00 a.m. (DEX group) or saline (CON group) once a day for 5 consecutive days were compared. Experimental hypercortisolism was confirmed by higher (p
ISSN:1734-1140
2299-5684
DOI:10.1016/S1734-1140(13)70972-1