1f:T4e1,Total parenteral nutrition with hypertonic glucose/AA solutions given to eighteen nutritionally depleted patients resulted in a rise in the respiratory quotient (RQ) from 0.83 to 1.05 (p less than .001), while oxygen consumption (VO2) increased only 3%. Excess glucose in depleted patients was converted to fat as evidenced by an RQ greater than 1.0. Administration of a similar glucose load to fourteen hypermetabolic patients (injury/infection) resulted in a rise in RQ from 0.76 to 0.90 while VO2 increased 29% (p less than .001) In hypermetabolic patients, even with administration of glucose in quantities above energy expenditure, there was still ongoing utilization of fat for energy, resulting in a RQ significantly less than 1.0. Excess glucose under these circumstances is apparently converted to glycogen while fat stores are utilized to partially meet energy needs. Septic and injuried man seems to preferentially utilize endogenous fat as an energy source. Administration of a large glucose load to hypermetabolic patients does not totally suppress the net fat oxidation as it does in depleted patients. Rather there is an increase in VO2, continuing oxidation of fat and apparently an increase in the conversion of glucose to glycogen.20:T45b,Total parenteral nutrition (TPN) using glucose as nonprotein calories was associated with increases in O₂consumption (V̇O₂) and CO₂production (V̇CO₂). The magnitude of the changes was a function of the patient's clinical state and glucose load. Depleted patients showed a minimal increase in V̇O₂, while V̇CO₂increased 23%. Minute ventilation (V̇_E) increased 32%. Hypermetabolic patients (major trauma, sepsis) had a 30% increase in VO₂and a 57% increase in V̇CO₂, while V̇_Eincreased 71%. Patients with mild to moderate injuries (energy expenditure ±15% of normal) showed a 21% increase in V̇O₂and a 53% increase in V̇CO₂, while V̇_Eincreased 121%. Large carbohydrate intakes were associated with increases in CO₂production in all patients, while increases in O₂consumption were seen primarily in hypermetabolic patients. These changes suggest that the high glucose loads of TPN may be a physiologic stress. (JAMA243:1444-1447, 1980)21:T956,

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