Hyperinsulinism in endotoxin shock dogs.

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.