Reticuloendothelial system function and glucose-insulin dyshomeostasis in sepsis.
Circulating glucose levels, peripheral glucose utilization, and hepatic gluconeogenesis were compared in late endotoxicosis and severe septic shock in rats. Endotoxin was administered intravenously as 5 mg of Salmonella enteritidis lipopolysaccharide B. Sepsis was induced in the peritoneal cavity by use of the cecal ligation and puncture technique. Late endotoxicosis and severe sepsis were comparable in hypoglycemia, increased peripheral glucose use, and depression of gluconeogenesis. Immunoreactive insulin was lower in endotoxicosis than in sepsis; both models demonstrated elevations in serum nonsuppressible insulin-like activity. Endotoxic pancreata secreted excessive insulin, as did pancreata obtained after blockade of the reticuloendothelial system (RES). Macrophage-conditioned media induced a hypersecretory state of the beta cells in donor pancreata. The RES serves as a source of secretory products, i.e., gluco-regulatory monokines, which affects insulinization of tissues in sepsis and thus underwrites the hypoglycemia of late endotoxicosis and severe sepsis.
D000818:Animals; D005947:Glucose / Q000378:metabolism*; D006706:Homeostasis; D007328:Insulin / Q000378:metabolism*; D012157:Mononuclear Phagocyte System / Q000378:metabolism*; D012377:Rodentia; D018805:Sepsis / Q000378:metabolism*; D012772:Shock, Septic / Q000378:metabolism*
D007328:Insulin; D005947:Glucose