|ITEM METADATA RECORD
|Title: ||Increasing intravenous glucose load in the presence of normoglycemia: effect on outcome and metabolism in critically ill rabbits|
|Authors: ||Derde, Sarah ×|
Van Herck, Erik
Van den Berghe, Greet #
|Issue Date: ||21-Nov-2009 |
|Conference: ||Belgian Endocrine Society's Annual Meeting edition:19 location:Brussels date:21 November 2009|
|Abstract: ||Aim: Endocrine disturbances and a feeding-resistant wasting-syndrome, characterized by a negative protein balance, promote delayed recovery and poor outcome of critical illness. Parenteral nutrition alone cannot counteract the hypercatabolic state, possibly in part due to aggravation of the hyperglycemic response to illness. In critically ill rabbits we investigated the impact of varying amounts of intravenous glucose, while maintaining normoglycemia, on mortality, organ damage, and markers of catabolism/anabolism.
Methods: Critically ill rabbits were randomized into a fasting group, a standard parenteral nutrition group, and two groups receiving either intermediate or high additional amounts of intravenous glucose within the physiological range, while maintained normoglycemic with insulin. These groups were compared with a hyperglycemic group that received a similar high glucose load as the last normoglycemic group, and with healthy rabbits. Protein and lipid load were equal for all fed groups.
Main results: Varying intravenous glucose load did not affect mortality or organ damage, provided hyperglycemia was prevented. Fasted critically ill rabbits lost weight, which was attenuated by increasing intravenous glucose load. As compared to healthy rabbits, mRNA expression and/or activity of several ubiquitin-proteasome-pathway components, cathepsin-L and calpain-1 was elevated in skeletal muscle of fasted critically ill rabbits. Intravenous feeding was able to counter-act this response. Excessive glucose load and/or hyperglycemia, however, reduced the protective effect of feeding. Genes investigated in diaphragm and myocardium revealed roughly a similar response. Except in the normoglycemic group with intermediate glucose load, circulating thyroid hormone and IGF-1 levels decreased, most pronounced in hyperglycemic rabbits.
Conclusions: Increasing intravenous glucose infusion within the physiological range, while maintaining normoglycemia, was safe for organ function and survival of critically ill rabbits. Concomitantly, it reduced the catabolic responses as compared with fasting. Whether this has a beneficial effect on muscle function and mass remains to be investigated.
|Publication status: ||published|
|KU Leuven publication type: ||AMa|
|Appears in Collections:||Laboratory for Intensive Care Medicine (-)|
Laboratory of Intensive Care Medicine
Animal Physiology and Neurobiology Section - miscellaneous
Clinical and Experimental Endocrinology
× corresponding author|
# (joint) last author|
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