Parenteral nutrition required following surgery or injury should not o
nly meet post-aggression caloric requirements but also match the speci
fic metabolic needs so as not to worsen the metabolic disruptions alre
ady present in this situation. The primary objective of parenteral nut
rition is body protein maintenance or restoration by reduction of prot
ein catabolism or promotion of protein synthesis or both. Whether all
parenteral energy donors, i.e., glucose, fructose, other polyols, and
lipid emulsions, are equally capable of achieving this objective conti
nues to be a controversial issue. The objective of the present study w
as to answer the following questions: (1) Do glucose and fructose diff
er in their effects on the metabolic changes seen following surgery or
injury, the changes in glucose metabolism in particular? (2) Can the
observation of poorer glucose utilization in the presence of lipids be
confirmed in ICU patients? Patients, materials and methods. A prospec
tive, randomized clinical trial has been conducted in 20 aseptic surgi
cal ICU patients to generate an objective database along these lines b
y performing a detailed analysis of the metabolic responses to differe
nt parenteral nutrition protocols. The effects of a glucose solution lipid emulsion regimen vs fructose solution + lipid emulsion regimen
on a number of carbohydrate and lipid metabolism variables were evalua
ted for an isocaloric (carbohydrates: 0.25 g/kg body weight/h; lipids:
0.166 g/kg body weight/h) and isonitrogenous (amino acids: 0.0625 g/k
g body weight/h) total nutrient supply over a 10-h study period. Resul
ts. A significantly smaller rise in blood glucose concentrations (incr
ease from baseline: glucose + lipids P < 0.001 vs fructose + lipids n.
s.) suggested that fructose had a small effect, if any at all, on gluc
ose metabolism. Serum insulin activity showed significant differences
as a function of carbohydrate regimen, i.e. infusion of fructose inste
ad of glucose produced a less pronounced increase in insulin activity
(increase from baseline: glucose + lipids P < 0.001 vs fructose/lipids
P < 0.01). Impairment of glucose utilization by concomitant administr
ation of lipids was observed neither in patients who first received gl
ucose nor in those who first received fructose. Conclusions. As demons
trated, parenteral fructose, unlike parenteral glucose, has a signific
antly less adverse impact than glucose on the glucose balance, which i
s disrupted initially in the post-aggression state. In addition, the l
ess pronounced increase in insulin activity during fructose infusion t
han during glucose infusion can be assumed to facilitate mobilization
of endogenous lipid stores and lipid oxidation. Earlier workers pointe
d out that any rise in free fatty acid and ketone body concentrations
in the serum produces inhibition of muscular glucose uptake and oxidat
ion, and of glycolysis. These findings were recorded in a rat model an
d could not be confirmed in our post-aggression state patients receivi
ng lipid doses commensurate with the usual clinical infusion rates. Th
e serious complications that can result from hereditary fructose intol
erance are completely avoidable if a cartful patient history is taken
before the first parenteral use of fructose. If the patient or family
members and close friends, are simply asked whether he/she can tolerat
e fruit and sweet dishes, hereditary fructose intolerance can be ruled
out beyond all reasonable doubt. Only in the extremely rare situation
s in which it is not possible to question either the patient or any si
gnificant other, a test dose will have to be administered to exclude f
ructose intolerance. The benefits of fructose-specific metabolic effec
ts reported in the literature and corroborated by the results of our o
wn study suggest that fructose is an important nutrient that contribut
es to metabolic stabilization, especially in the post-aggression phase
and in septic patients. Hyperglycaemic states are largely prevented,
and fewer patients require exogenous insulin, thus avoiding the freque
ntly underestimated risk of hypoglycaemic states.