International Congress on Prediabetes and the Metabolic Syndrome edition:3 location:Nice date:1-4 April 2009
Endocrine disturbances during critical illness lead to a feeding-resistant wasting-syndrome,
characterised by profound protein breakdown, promoting delayed recovery and poor outcome.
Parenteral nutrition failed to counteract the hypercatabolic state, possibly due to aggravation of the
detrimental hyperglycemic response to critical illness. In our rabbit model of prolonged critical illness
we investigated the impact of varying intravenous glucose load, while maintaining normoglycemia, on
mortality, organ damage, and catabolism/anabolism.
Critically ill rabbits were randomised into a fasting group, a standard parenteral nutrition group, and
two groups receiving either an intermediate or high additional amount of intravenous glucose within
the physiological range, all maintained normoglycemic with insulin. These normoglycemic groups
were compared with a hyperglycemic group (similar high glucose load as the last normoglycemic
group) and with healthy rabbits. Protein and lipid load was equal for all fed groups.
Varying intravenous glucose load did not affect mortality or organ damage, provided normoglycemia
was maintained. Fasted critically ill rabbits lost weight, which was attenuated by increasing
intravenous glucose load. As compared to healthy rabbits, mRNA expression of several components
of the ubiquitin-proteasome-pathway was elevated in skeletal muscle of fasted critically ill rabbits,
which was counteracted by intravenous feeding. Except in the normoglycemic group with
intermediate glucose load, circulating IGF-1 and thyroid hormone levels decreased in all groups,
most pronounced in hyperglycemic rabbits.
Provided normoglycemia is maintained, increasing intravenous glucose within the physiological
range is safe for organ function and survival of critically ill rabbits and reduces catabolism compared