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  • Poster presentation
  • Open Access

Alterations in adipose tissue during critical illness: an adaptive and protective response?

  • 1,
  • 1,
  • 1,
  • 1,
  • 1,
  • 2,
  • 2 and
  • 1
Critical Care201014 (Suppl 1) :P591

https://doi.org/10.1186/cc8823

  • Published:

Keywords

  • Adipose Tissue
  • Matched Control
  • Critical Illness
  • Toxic Metabolite
  • Glucose Content

Introduction

Critical illness is characterized by lean tissue wasting whereas adipose tissue is preserved. Obese critically ill patients may have a lower risk of death than nonobese patients, a recent observation that may suggest a protective role for adipose tissue during illness, a role which has not been previously investigated. We hypothesized that adipose tissue could function as a waste bin for potentially toxic metabolites, such as glucose, during critical illness.

Methods

We studied adipose tissue biopsies from 61 of critically ill patients, more specifically morphology and the potential to take up and metabolize glucose, and compared this with biopsies from 20 matched controls.

Results

Adipose tissue biopsies from critically ill patients revealed a higher number and a smaller size of adipocytes as compared with matched controls, coinciding with increased preadipocyte marker levels. Also, >95% of adipose biopsies from critically ill patients displayed positive macrophage staining. Gene and protein expression of insulin-independent GLUTs, and tissue glucose content was increased. Glucokinase expression was upregulated whereas glycogen and glucose-6-phosphate levels were low. Acetyl-CoA-carboxylase protein level and activity of fatty-acid synthase were increased. A substantially increased activity of AMPK may play a crucial role.

Conclusions

The larger number of small adipocytes in response to critical illness appears to have an increased ability to take up and metabolize glucose into fatty acids. Such changes may render adipose tissue biologically active as a functional waste bin for toxic metabolites during critical illness, which could contribute to survival.

Authors’ Affiliations

(1)
KU Leuven, Leuven, Belgium
(2)
Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK

Copyright

© BioMed Central Ltd. 2010

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