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- W1978515097 abstract "Objective To review the possible mechanisms for the reported clinical finding of better outcomes for hospitalized and critically ill patients as the result of improved metabolic control. Results Insulin inhibits free fatty acids, proinflammatory cytokines, and inflammatory growth factors, all of which may be detrimental in critically ill patients. Furthermore, insulin enhances nitric oxide synthesis, which promotes vasodilation. The mechanisms of insulin regulation of these factors are complex, although insulin seems to have a direct effect on the transcriptional factor, nuclear factor-κβ (NF-κβ). In turn, NF-κβ modulates the proinflammatory cytokines, adhesion molecules, and chemokines. In a euglycemic or slightly hyperglycemic environment, NF-κβ is suppressed by insulin; however, with more profound hyperglycemia, NF-κβ is induced and the proinflammatory cytokines are thus increased. Conclusion Although considerable research must be completed to identify the apparent relationship between stringent metabolic control and improved outcomes in acutely ill patients, current evidence suggests that both the treatment (glucose-insulin-potassium infusion) and the resultant plasma glucose concentrations may be independent important components of the underlying mechanisms. (Endocr Pract. 2004;10[Suppl 2]:63-70)" @default.
- W1978515097 created "2016-06-24" @default.
- W1978515097 creator A5029280234 @default.
- W1978515097 date "2004-03-01" @default.
- W1978515097 modified "2023-10-11" @default.
- W1978515097 title "Effect of Insulin Therapy on Nonglycemic Variables During Acute Illness" @default.
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- W1978515097 doi "https://doi.org/10.4158/ep.10.s2.63" @default.
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