[Fat infusion and carbohydrate metabolism].

In non-insulin-dependent diabetics (type II), in obese patients and in critically ill patients, there is an insulin resistant metabolic state. The mechanism of insulin resistance can be defined in states of reduced insulin sensitivity of the receptor, reduced insulin responsiveness, and a combination of these two hormone resistant states. The molecular mechanism or the insulin resistance may be localized prior to the interaction of insulin with the receptors (pre-receptor defect), alteration of the interaction of insulin with its receptor, and disorders associated with the alteration of the intracellular steps in insulin action (post-receptor defect). In acutely ill patients the number of insulin receptors are diminished and a reduced sensitivity and reduced responsiveness of the metabolism to insulin action may result. At the intracellular level there is an inhibition of the phosphofructokinase and the pyruvatedehydrogenase complex. In this given metabolic state fatty acids are preferentially metabolized, which may be supported by intravenous fat. Later, if no special restrictions against the lipid component are given, the parenteral nutrition should use all the three main components: lipids, glucose and amino acids.