Adaptation of glucose production and gluconeogenesis to diminishing glucose infusion in preterm infants at varying gestational ages.
In preterm infants low plasma glucose concentrations are frequently observed. We hypothesized that the infants' ability to adapt endogenous glucose production to diminishing exogenous supply is disturbed, but will improve with increasing gestational age. Glucose production rate and gluconeogenesis were measured using stable isotope techniques with [6,6-2H2]glucose and [2-13C]glycerol in 19 preterm infants (10 < or = 30 wk and nine >30 wk gestational age) on d 5.0 +/- 1.4 of life. Exogenous glucose was administered at a rate of 33 micromol x kg-1 x min-1 followed by 22 micromol x kg-1 x min-1. In the first 2 h after the decrease in exogenous supply, plasma glucose concentration declined comparably in both groups: < or =30 wk, from 4.3 +/- 1.2 to 3.2 +/- 0.9 mM; >30 wk, from 3.7 +/- 0.7 to 3.0 +/- 0.6 mM. Thereafter, only in infants >30 wk an increase was observed, to 3.4 +/- 0.8 mM. Glucose production rate increased comparably in both groups: < or =30 wk, from 6.0 +/- 4.1 to 8.8 +/- 3.4 micromol x kg-1 x min-1; >30 wk, from 7.8 +/- 4.6 to 11.6 +/- 5.2 micromol x kg-1 x min-1. This increase was equivalent to approximately 30% of the decline in exogenous glucose. Gluconeogenesis increased comparably in both groups: <30 wk, from 3.2 +/- 1.2 to 4.5 +/- 1.3 micromol x kg-1 x min-1; >30 wk, from 4.3 +/- 1.9 to 6.8 +/- 2.9 micromol x kg-1 x min-1. We conclude that preterm infants can only partly compensate a decline in exogenous glucose supply by increasing endogenous glucose production rate, probably because of limitations in the final common pathway of intracellular glucose metabolism (i.e. glucose-6-phosphatase). The ability to maintain the plasma glucose concentration after a decrease in exogenous supply is better preserved in infants >30 wk owing to more efficient adaptation of peripheral glucose utilization.
Van Kempen
Anne A M W
AA
Metabolism Unit, Department of Endocrinology and Metabolism, Emma Children's Hospital, Amsterdam, The Netherlands. A.vanKempen@amc.uva.nl
Romijn
Johannes A
JA
Ruiter
An F C
AF
Ackermans
Mariette T
MT
Endert
Erik
E
Hoekstra
J Hans
JH
Kok
Johanna H
JH
Sauerwein
Hans P
HP
D000409:Alanine / Q000097:blood; D005230:Fatty Acids, Nonesterified / Q000097:blood; D005260:Female; D005865:Gestational Age; D005943:Gluconeogenesis / Q000187:drug effects* / Q000502:physiology*; D005947:Glucose / Q000008:administration & dosage* / Q000096:biosynthesis* / Q000493:pharmacokinetics; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007231:Infant, Newborn; D007234:Infant, Premature / Q000378:metabolism*; D007262:Infusions, Intravenous; D007328:Insulin / Q000097:blood; D008297:Male
D005230:Fatty Acids, Nonesterified; D007328:Insulin; D005947:Glucose; D000409:Alanine; D006854:Hydrocortisone