Excessive glucose administration in severe septic patients: a possible cause of fatty degeneration in skeletal muscle tissue

Abstract The ability to oxidise fatty acids was found to be impaired in severe septic patients with multiple organ failure. Thus, glucose still represents the major substrate for total parenteral nutrition in such conditions. To evaluate the effect of a high glucose load on peripheral substrate metabolism (priming dose: 10 g/5 min, constant infusion rate: 0.5g/kg·h) we studied muscle metabolism in five patients with hypodynamic septic shock (S) using the forearm technique. Data were compared to those of five patients 3 h after elective surgery (O), who were believed to show the typical metabolic pattern of a compensated stress response. Arterial and deep venous concentrations of glucose, lactate, pyruvate, acetoacetate (AcAc), β-hydroxbutyrate (β-HOB), free fatty acids (FFA), glycerol, oxygen, insulin, adrenalin and noradrenalin were determined in the basal period and during glucose infusion. Consistent with an impaired mobilisation of endogenous substrate stores basal arterial concentrations of FFA, β-HOB and AcAc were markedly lower in severe sepsis. In O glucose infusion resulted in a continuous increase of forearm glucose uptake, compensating falling rates of FFA and ketone body uptake due to decreased arterial supply. On the contrary, in S arterial supply of FFA, AcAc and β-HOB almost remained unchanged during glucose infusion. Nevertheless, muscular balances of FFA were affected significantly, changing from a basal release into uptake during glucose infusion (basal: −0.23 ± 0.17 μmol/100 g min; 10 min of glucose infusion: 0.30 ± 0.31; 20 min: 0.95 + 0.92 ∗ ; 40 min: 0.32 ± 0.26 ∗ ; ∗ : p Thus peripheral lipogenesis might arise from excessive glucose administration in such conditions due to an increased rate of muscular re-esterification of FFA. To avoid this adverse side effect administration of glucose calories should be limited to basal energy requirements.