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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #138301

Title: PARENTERAL GLYCEROL ENHANCES GLUCONEOGENESIS IN VERY PREMATURE INFANTS

Author
item Sunehag, Agneta

Submitted to: Pediatric Research
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/13/2002
Publication Date: 4/1/2003
Citation: Sunehag AL. Parenteral Glycerol Enhances Gluconeogenesis in Very Premature Infants. 2003 Pediatr Res 53:635-641.

Interpretive Summary: Very premature infants are dependent on feeding by vein during the first weeks of life. A problem is that they have a low tolerance for sugar given by vein, which very often results in too high blood sugar concentrations. We have previously demonstrated that very premature infants receiving sugar at a rate corresponding to about half their normal sugar turnover rate plus fat and amino acid solutions given by vein, maintain normal blood sugar values by using their metabolic pathway to produce sugar from fat and amino acids (a process called gluconeogenesis). We have also demonstrated that the fat solution is more important than the amino acid solution in supporting gluconeogenesis. The fat solution contains glycerol, which can be used directly as a substrate for gluconeogenesis, but also fatty acids, which can drive the gluconeogenic process. In order to determine the individual effects of these two components, in the present study, very premature infants were given glycerol by vein. Our results demonstrate that in these small infants, glycerol was used for production of sugar. The rates of gluconeogenesis observed in infants receiving only glycerol were comparable to those observed in infants receiving the fat emulsion, containing both glycerol and fatty acids. Thus, we conclude that glycerol is the most important component of the lipid emulsion in supporting gluconeogenesis in very premature infants.

Technical Abstract: 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 wks) were studied on d 4 ± 1 (mean ± SE). All infants received glucose at 17 mmol/kg min during 9 h (following a first study h with 33 mmol/kg min). Eight infants received no additional substrate during the study, while 12 infants received supplemental glycerol at 5 (n=6) or 10 mmol/kg min (n=6) over the last 5 h of study. In infants receiving glucose alone, between Period 1 (study h 4-5) and Period 2 (study h 9-10), rates of glucose production decreased from 12.9 ± 1.2 to 7.4 ± 0.9 mmol/kg.min (p<0.01). This was the result of decreased glycogenolysis but no change in gluconeogenesis (5.1 ± 0.6 vs. 5.7 ± 0.4 mmol/kg min) (ns). Glycerol infusion at 5 and 10 mmol/kg 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 mmol/kg min, (p<0.01). Conclusion: In very premature infants, parenteral glycerol enhances gluconeogenesis and attenuates time dependent decrease in glucose production.