title: Hyperinsulinism in endotoxin shock dogs.
abstract: Extreme hyperinsulinism was observed in endotoxin-shock dogs made hyperglycemic by glucose infusion. Qualitatively (at least in terms of gel filtration characteristics), the insulin secreted under these conditions was normal. Hyperinsulinism was not observed in endotoxin-shock dogs not given glucose. Thus hyperinsulinism does not explain the hypoglycemia so frequently observed in endotoxin-treated dogs. Hyperinsulinsm could not be impaired degradation of insulin as disappearance of labeled insulin as well as cold insulin was comparable in control and endotoxin-treated animals. An adrenergic mechanism (either beta receptor stimulation or postadrenergic hyperresponsiveness of the beta cells) probably does not explain the hyperinsulinism observed in endotoxin-shock dogs given glucose as beta blockade failed to inhibit the hyperinsulinsm. Hyperinsulinism was not observed in endotoxin-shock dogs given tolbuamide. A tenfold rise in plasma IRG was observed in endotoxin-treated dogs whether glucose was infused or not. The persistently low IRI levels in endotoxin-treated dogs not given glucose suggest that hyperresponsiveness of the beta cell to glucagon was not present in these animals. Extreme hyperinsulinsm in response to induced hyperglycemia in endotoxin-shock dogs is unexplained. Hyperresponsiveness of the beta cell to glucose during endotoxin shock seems likely.
mesh_terms: D000496:Alloxan / Q000494:pharmacology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D004285:Dogs; D004926:Escherichia coli; D005947:Glucose / Q000494:pharmacology; D006946:Hyperinsulinism / Q000209:etiology*; D007515:Islets of Langerhans / Q000187:drug effects; D011433:Propranolol / Q000494:pharmacology; D011941:Receptors, Adrenergic; D012772:Shock, Septic / Q000150:complications*; D014044:Tolbutamide / Q000494:pharmacology
chemical_list: D001786:Blood Glucose; D011941:Receptors, Adrenergic; D000496:Alloxan; D014044:Tolbutamide; D011433:Propranolol; D005947:Glucose