Journal of Leukocyte Biology eBioscience full spectrum cell analysis
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

A more recent version of this article appeared on March 1, 2004

Published online before print December 4, 2003
This Article
Right arrow Full Text (Reprint (PDF))
Right arrow All Versions of this Article:
jlb.0503195v1
75/3/413    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Andersen, S. K.
Right arrow Articles by Tønnesen, E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Andersen, S. K.
Right arrow Articles by Tønnesen, E.
© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0503195

Received for publication May 1, 2003.
Revised October 14, 2003.
Accepted for publication October 21, 2003.

Article

The roles of insulin and hyperglycemia in sepsis pathogenesis

Soren Kaeseler Andersen @, Jakob Gjedsted , Christian Christiansen , and Else Tønnesen

Deparment of Anestesiology and Intensive Care, Institute of Experimental Clinical Research. Aarhus University Hospital, Denmark

@ To whom correspondence should be addressed. E-mail: ska{at}akhphd.au.dk.


  Abstract

Hyperglycemia is a risk marker of morbidity and mortality in acute, critical illness, and insulin therapy seems to be beneficial in this patient group. Whether this is true for a population of sepsis patients, as such, has not been investigated in clinical trials, but evidence from in vitro studies and experimental sepsis suggests that this may be the case. The endocrinology of septic patients is characterized by a shift in the balance between insulin and its counter-regulatory hormones favoring the latter. This leads to prominent metabolic derangements composed of high release and low use of glucose, amino acids, and free fatty acids (FFA), resulting in increased blood levels of these substrates. Circulating, proinflammatory mediators further enhance this state of global catabolism. Increased levels of glucose and FFA have distinct effects on inflammatory signaling leading to additional release of proinflammatory mediators and endothelial and neutrophil dysfunction. Insulin has the inherent capability to counteract the metabolic changes observed in septic patients. Concomitantly, insulin therapy may act as a modulator of inflammatory pathways inhibiting the unspecific, inflammatory activation caused by metabolic substrates. Given these properties, insulin could conceivably be serving a dual purpose for the benefit of septic patients.

Key Words: metabolism • endocrinology • stress hyperglycemia • septic shock • immunology • inflammation




This article has been cited by other articles:


Home page
 Am. J. Physiol. Renal Physiol.Home page
S. Basi, L. B. Pupim, E. M. Simmons, M. T. Sezer, Y. Shyr, S. Freedman, G. M. Chertow, R. L. Mehta, E. Paganini, J. Himmelfarb, et al.
Insulin resistance in critically ill patients with acute renal failure
Am J Physiol Renal Physiol, August 1, 2005; 289(2): F259 - F264.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Copyright © 2003 by the Society for Leukocyte Biology.