The influence of diabetic state on endotoxicosis.
Bacterial endotoxins deplete glycogen reserves in the host, oppose the gluconeogenic action of steroid hormones, and lower energy reserves in mammals. For the past 50 years the intermediary metabolism has been regarded as causal to the eventual outcome of endotoxicosis. Whereas some diabetogenic agents such as streptozotocin actually enhance the toxic effects of endotoxins, others (alloxan) do not appear to influence this parameter. Force feeding of glucose does not alter the outcome of endotoxicosis. Yet, endotoxins are believed to elicit insulin-like mediators from macrophages. In addition, the C3H/HeJ strain of mice which exhibits refractoriness to the lethal effects of the toxin undergoes just as severe a loss in total glycogen reserves as Swiss albino mice which are highly sensitive to endotoxin mediated death. These and similar observations suggest that the prime target(s) in endotoxicosis still remain elusive. However, endotoxins appear to form an important and interesting tool to elucidate various aspects of host physiology.
Lazar
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Agarwal
M K
MK
D000818:Animals; D001424:Bacterial Infections / Q000150:complications / Q000503:physiopathology*; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000503:physiopathology*; D004731:Endotoxins / Q000008:administration & dosage; D005938:Glucocorticoids / Q000494:pharmacology; D005943:Gluconeogenesis / Q000187:drug effects; D005947:Glucose / Q000494:pharmacology; D006019:Glycolysis / Q000187:drug effects; D008099:Liver / Q000378:metabolism; D008112:Liver Glycogen / Q000378:metabolism; D008757:Methylglucosides / Q000494:pharmacology; D051379:Mice; D051381:Rats; D013311:Streptozocin / Q000494:pharmacology
D004731:Endotoxins; D005938:Glucocorticoids; D008112:Liver Glycogen; D008757:Methylglucosides; D013311:Streptozocin; D005947:Glucose