TY - JOUR
T1 - Alanine administration does not stimulate gluconeogenesis in preterm infants
AU - van Kempen, Anne A. M. W.
AU - Romijn, Johannes A.
AU - Ruiter, An F. C.
AU - Endert, Erik
AU - Weverling, Gerrit Jan
AU - Kok, Johanna H.
AU - Sauerwein, Hans P.
PY - 2003
Y1 - 2003
N2 - Gluconeogenesis partially depends on sufficient precursor supply, and plasma alanine concentrations are generally low in preterm infants. Stimulation of gluconeogenesis may contribute to the prevention of hypoglycemia, an important clinical problem in these infants. In this study we evaluated the effect of extra precursor supply on gluconeogenesis in preterm infants. In 11 infants, gestational age less than or equal to 32 weeks, glucose production rate (GPR) and gluconeogenesis were measured using the [6,6(_2) H-2]glucose dilution technique and mass isotopomer distribution analysis with [2-C-13]glycerol, respectively. Unlabeled glucose was administered throughout the study period at a rate of 22 mumol (.) kg(-1) (.) min(-1). Five infants received alanine (1.5 mg (.) kg(-1) (.) min(-1)) during the last 3 hours of the study protocol, and 6 infants served as controls. In the control group the rate of gluconeogenesis and GPR remained constant at 4.0 +/- 0.3 mumol (.) kg(-1) (.) min(-1) and 8.3 +/- 0.6 mumol (.) kg(-1) (.) min(-1), respectively. In the alanine group plasma alanine concentrations increased from 45 +/- 23 to 829 +/- 115 mumol/L [P = .001); gluconeogenesis and GPR did not differ from control: 3.8 +/- 0.2 mumol (.) kg(-1) (.) min(-1) and 6.4 +/- 2.0 mumol (.) kg(-1) (.) min(-1), respectively. We conclude that administration of the gluconeogenic precursor alanine does not stimulate gluconeogenesis in preterm infants, despite a sharp increase in plasma alanine concentrations. We speculate either a restricted capacity of the enzymes involved in the gluconeogenic pathway or a low secretion rate of glucoregulatory hormones as causative mechanisms involved in the gluconeogenic pathway in the preterm neonate. (C) 2003 Elsevier Inc. All rights reserved
AB - Gluconeogenesis partially depends on sufficient precursor supply, and plasma alanine concentrations are generally low in preterm infants. Stimulation of gluconeogenesis may contribute to the prevention of hypoglycemia, an important clinical problem in these infants. In this study we evaluated the effect of extra precursor supply on gluconeogenesis in preterm infants. In 11 infants, gestational age less than or equal to 32 weeks, glucose production rate (GPR) and gluconeogenesis were measured using the [6,6(_2) H-2]glucose dilution technique and mass isotopomer distribution analysis with [2-C-13]glycerol, respectively. Unlabeled glucose was administered throughout the study period at a rate of 22 mumol (.) kg(-1) (.) min(-1). Five infants received alanine (1.5 mg (.) kg(-1) (.) min(-1)) during the last 3 hours of the study protocol, and 6 infants served as controls. In the control group the rate of gluconeogenesis and GPR remained constant at 4.0 +/- 0.3 mumol (.) kg(-1) (.) min(-1) and 8.3 +/- 0.6 mumol (.) kg(-1) (.) min(-1), respectively. In the alanine group plasma alanine concentrations increased from 45 +/- 23 to 829 +/- 115 mumol/L [P = .001); gluconeogenesis and GPR did not differ from control: 3.8 +/- 0.2 mumol (.) kg(-1) (.) min(-1) and 6.4 +/- 2.0 mumol (.) kg(-1) (.) min(-1), respectively. We conclude that administration of the gluconeogenic precursor alanine does not stimulate gluconeogenesis in preterm infants, despite a sharp increase in plasma alanine concentrations. We speculate either a restricted capacity of the enzymes involved in the gluconeogenic pathway or a low secretion rate of glucoregulatory hormones as causative mechanisms involved in the gluconeogenic pathway in the preterm neonate. (C) 2003 Elsevier Inc. All rights reserved
U2 - https://doi.org/10.1016/S0026-0495(03)00148-3
DO - https://doi.org/10.1016/S0026-0495(03)00148-3
M3 - Article
C2 - 12898456
SN - 0026-0495
VL - 52
SP - 945
EP - 949
JO - Metabolism: Clinical and Experimental
JF - Metabolism: Clinical and Experimental
IS - 8
ER -