Dexamethasone antagonism of glucose dyshomeostasis in endotoxin shock.
Dexamethasone acetate (100 microgram IP) protected male Holtzman rats (300-330 gm) against endotoxin shock due to Salmonella enteritidis lipopoly-saccharide B IV. Endotoxin (5.0 mg/rat) produced hypoglycemia within 180 minutes, ie, plasma glucose fell from 87 to 24 mg/dl; dexamethasone prevented the hypoglycemia, ie, plasma glucose levels were 129 mg/dl at 180 minutes after endotoxin. Dexamethasone antagonized both endotoxin-induced depression of hepatic gluconeogenesis and enhanced glucose oxidation as evaluated in vivo. Epididymal fat pads from endotoxic rats (100-110 gm) had increased rates of glucose oxidation as evaluated by the in vitro conversion of 14C-D-glucose to 14CO2. Dexamethasone both in vivo and in vitro antagonized endotoxin glucose hypercatabolism by isolated epididymal fat pads following administrated of endotoxin. Glucocorticoid protection against endotoxin shock is related to antagonism of glucose dyshomeostasis.
D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D003907:Dexamethasone / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism*; D006008:Glycogen Storage Disease; D008297:Male; D051381:Rats; D012772:Shock, Septic / Q000378:metabolism*
D003907:Dexamethasone; D005947:Glucose