ARS | Publication request: Gluconeogenesis continues in premature infants receiving total parenteral nutrition

Submitted to: Trade Journal Publication
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: February 15, 2010
Publication Date: November 1, 2010
Citation: Chacko, S.K., Sunehag, A.L. 2010. Gluconeogenesis continues in premature infants receiving total parenteral nutrition. Archives of Disease in Childhood, Fetal & Neonatal Edition. 95(6):F413-F418.

Interpretive Summary: Infants born prematurely are at high risk of disturbed sugar metabolism, particularly during their first week of life when they are dependent on nutrition (sugar, fat, and protein) by vein. These infants are often receiving sugar by vein at high infusion rates, which results in a frequent occurrence of high blood sugar concentrations. This can have negative effects on their short and long term clinical outcome. The purpose of this study was to determine, whether the production of new sugar (gluconeogenesis) in the liver continues even when the infants receive sugar by vein at rates exceeding their requirements in addition to fat and protein. We studied eight infants born after an average of 26.5 weeks and with birth weights averaging 1 kg. The results of the study show that production of new sugar continues despite the sugar supply exceeded the estimated requirements. Further, blood sugar concentrations were directly related to the amount of sugar given by vein. Since the body’s own production of sugar can obviously not be regulated, the best way to prevent high blood sugar is to adjust the sugar infusion to the infants’ requirements.

Technical Abstract: To determine the contribution of total gluconeogenesis, to glucose production in preterm infants receiving total parenteral nutrition (TPN) providing glucose exceeding normal infant glucose turnover rate, eight infants (0.955 +/- 0.066 kg, 26.5 - 0.5 wks, 4-1 d) were studied while receiving routine TPN. Glucose appearance rate (Ra) (the sum of rates of glucose infusion and residual glucose production), and gluconeogenesis were measured by stable isotope-GCMS techniques using deuterated water and applying the Chacko et. al. as well as the Landau et. al. methods. Blood glucose ranged from 5.2 to 14.3 mmol/L (94 to 257 mg/dl) and glucose infusion rate from 7.4 to 11.4 mg/kg.min, thus exceeding the normal glucose production rates of newborn infants in most of the babies. Glucose Ra was 12.4 +/- 0.6 and GPR 2.1 +/- 0.3 mg/kg.min. Gluconeogenesis as a fraction of glucose Ra was 11.2 +/- 1.1% (Chacko et. al) and 10.5 +/- 1.2% (Landau et. al) (NS) and the rate of gluconeogenesis 1.35 +/- 0.15 mg/kg.min (Chacko et. al) and 1.29 +/- 0.14 mg/kg.min (Landau et. al) (NS). Gluconeogenesis accounted for 73 +/- 11% and 68 +/- 10 (NS) of the glucose production rate for the two methods, respectively. Gluconeogenesis and glycogenolysis were not affected by total glucose infusion rate, glucose concentration, gestational age, or birth weight. Glucose concentration correlated with total glucose infusion rate and gestational age (combined R2=0.79, p=0.02). Gluconeogenesis is sustained in preterm infants receiving routine TPN providing glucose at rates exceeding normal infant glucose turnover rate, and accounts for the major part of residual glucose production. Gluconeogenesis is not affected by glucose infusion rate or blood glucose concentration.