Parenteral glycerol enhances gluconeogenesis in very premature infants.

We have previously demonstrated that very premature infants receiving total parenteral nutrition maintain normoglycemia primarily by glucose produced via gluconeogenesis and that the lipid emulsion is most important in supporting gluconeogenesis. It is, however, not clear whether this is a result of the glycerol or the fatty acid constituent. The purpose of the present study was to determine the effect of intravenous supplemental glycerol alone on glucose production and gluconeogenesis. Twenty infants (birth weight, 1014 +/- 32 g; gestational age, 27 +/- 1 wk) were studied on d 4 +/- 1 (mean +/- SE). All infants received glucose at 17 micromol/kg x min for 9 h (after an initial study hour with 33 micromol/kg x min). Eight infants received no additional substrate during the study, and 12 infants received supplemental glycerol at 5 (n = 6) or 10 micromol/kg x min (n = 6) over the last 5 h of study. In infants receiving glucose alone, between period 1 (study hours 4-5) and period 2 (study hours 9-10), rates of glucose production ([U-13C]glucose) decreased from 12.9 +/- 1.2 to 7.4 +/- 0.9 micromol/kg x min (p < 0.01). This was the result of decreased glycogenolysis but no change in gluconeogenesis ([U-13C]glucose mass isotopomer distribution analysis) (5.1 +/- 0.6 versus 5.7 +/- 0.4 micromol/kg x min) (ns). Glycerol infusion at 5 and 10 micromol/kg x min, respectively, maintained glucose production (despite comparable decrease in glycogenolysis) by increasing gluconeogenesis from 4.3 +/- 0.2 to 6.3 +/- 0.5 (p < 0.03), and 6.0 +/- 0.7 to 8.8 +/- 0.8 micromol/kg/min (p < 0.01). In very premature infants, parenteral glycerol enhances gluconeogenesis and attenuates time dependent decrease in glucose production.