Alanine administration does not stimulate gluconeogenesis in preterm infants.

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 < or = 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-(13)C]glycerol, respectively. Unlabeled glucose was administered throughout the study period at a rate of 22 micromol. 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 micromol. kg(-1). min(-1) and 8.3 +/- 0.6 micromol. kg(-1). min(-1), respectively. In the alanine group plasma alanine concentrations increased from 45 +/- 23 to 829 +/- 115 micromol/L (P =.001); gluconeogenesis and GPR did not differ from control: 3.8 +/- 0.2 micromol. kg(-1). min(-1) and 6.4 +/- 2.0 micromol. 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.