Under normal circumstances there is a reciprocal relation between the avail
ability of free fatty acids (FFAs) and glucose in plasma. In the fasted sta
te, FFAs predominate in both availability and the relative contribution to
energy production, whereas the same is true for glucose in the fed state. T
he extent of glucose oxidation is directly determined by its availability,
whereas FFAs are normally available well in excess of their rate of oxidati
on. The rate of FFA oxidation is determined by the rate of transfer into th
e mitochondria via the carnitine palmitoyltransferase (CPT) enzyme system,
which in turn is regulated by the metabolism of glucose. With critical illn
ess the stress response involves mobilization of both plasma glucose and FF
As simultaneously in both the fed and fasted states. In the situation of ex
cess availability of substrates, the metabolism of glucose limits the oxida
tion of FFAs, thereby channeling those fatty acids into triglyceride (TG) s
tores in the muscle and the Liver. The high FFA concentrations and increase
d tissue TG stores can Limit glucose clearance from the blood, thereby cont
ributing to the development of hyperglycemia. Also, the excessive metabolis
m of glucose can result in lacticacidemia and can contribute to the depleti
on of muscle glutamine. The nutritional treatment of such patients must acc
ount for these underlying metabolic responses to avoid amplifying potential
ly detrimental responses to the excess availability of substrates already p
resent in the fasting stale.