There may be any number of molecular and/or cellular mechanisms
to explain the decreased risk of pneumonia observed in
patients receiving a high-carbohydrate enteral feeding regimen
compared to those receiving a high-fat enteral feeding regimen.
Most immune systemcells are obligate glucose consumers (Deitch
1995), and research suggests rates of glycolysis may nearly double
in severely burned patients (Gore 2001; Wolfe 1979). High-carbohydrate
enteral feeding regimens may supply glucose required
by highly active immune system cells. Likewise, inadequate provision
of dietary glucose may limit intracellular availability and subsequently
impair immune system function. It is well established
that chronic hyperglycaemia inhibits wound healing and increases
the risk of infectious complications in the intensive care setting