Increased insulin responsiveness in endotoxicosis.
The relation of endotoxicosis to insulin responsiveness was evaluated in male Holtzman rats. Salmonella enteritidis lipopolysaccharide at 0.5 or 1.0 mg per 300 g rat increased lethality in convulsive seizure deaths to 0.25, 0.50, or 1.0 U insulin sc. The hypoglycemic nadir induced by 0.05, 0.10, or 0.25 U of insulin sc was greater in rats rendered endotoxic with 1 mg of lipopolysaccharide IV. Oxidation of U-14C-D-glucose to 14 CO2 by endotoxic tissues in vitro was augmented in liver slices, epididymal fat pads, hemidiaphragms, and spleen slices; no pronounced glucose oxidation increases occurred in lung, heart, stomach, cerebrum, kidney, or whole blood. Epididymal fat pads from endotoxic rats (100 g) manifested increased basal glucose oxidation as well as an enhanced maximal response to incremental insulin doses of 0.01 to 25 mU/ml. It is suggested that altered tissue responsiveness in concert with hyperinsulinemia underlie the profound alterations in glucose homeostasis during endotoxicosis.
D000818:Animals; D005947:Glucose / Q000378:metabolism; D007003:Hypoglycemia / Q000150:complications*; D066298:In Vitro Techniques; D007328:Insulin / Q000502:physiology*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D051381:Rats; D011919:Rats, Inbred Strains; D012477:Salmonella enteritidis; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*
D007328:Insulin; D008070:Lipopolysaccharides; D005947:Glucose