Normal postnatal glucose homeostasis is established by increased
glucose production and glucose utilization.1 Factors
that promote glucose production and release into the circulation
include catecholamines and glucagon, which activate glycogenolysis.
A high glucagon-to-insulin ratio, which induces synthesis and activity
of the enzymes, is required for gluconeogenesis. Once normal feedings
are established, glycerol and amino acids continue to fuel gluconeogenesis
while dietary fatty acids activate the enzymes responsible for gluconeogenesis.
Additionally, galactose derived from hydrolysis of milk sugar (lactose)
in the gut increases hepatic glycogen production for sustained between-feeding hepatic
glucose release from glycogen breakdown. Feedings also induce production
of intestinal peptides, or incretins, that promote insulin secretion.
Insulin decreases hepatic glucose production and increases glucose
utilization for energy production and storage as glycogen. These
opposing conditions of glucose production and utilization continue
in response to normal feed-fast cycles, regulating normal plasma
Glucose is the major source of energy for organ function. All
organs use glucose, and glucose deficiency leads to impaired cardiac performance,
cerebral energy failure, hepatic glycogen depletion, and muscle
weakness.3 Cerebral glucose metabolism accounts
for as much as 90% of total glucose consumption in the
newborn. Thus, maintenance of glucose delivery to all organs, particularly
the brain, is an essential physiological function.4 Although alternate
fuels can substitute for glucose metabolism, concentrations of these
substances often are low in newborn infants, especially preterm
infants. Newborns, therefore, are especially susceptible to hypoglycemia
when they are exposed to conditions that impair glucose homeostasis
during the transition from intrauterine to extrauterine life.
Hypoglycemia ought to be defined as any glucose
concentration below the lower limit of the normal range of blood
or plasma/serum glucose concentrations.5 This
concentration, however, is uncertain, controversial, and variably
defined. Early statistical evaluations in term infants defined hypoglycemia
as a blood glucose concentration below 35 mg/dL, or a plasma
glucose value below 40 mg/dL; even lower concentrations
were used to define hypoglycemia in preterm infants. Such statistical definitions,
however, have limited biological or clinical significance, as physiologically
hypoglycemia is present when the concentration of glucose in the
plasma produces glucose delivery rates that are inadequate to meet
essential requirements for glucose utilization. Such requirements
vary considerably among infants and over a broad range of glucose
concentrations. Definitions of normal and hypoglycemic glucose concentrations
also depend on postnatal feeding practices and when birth glucose
concentrations are measured. Glucose concentrations are higher,
for example, when feedings are initiated soon after birth than when
feedings are delayed for several hours. Postnatally, the blood glucose
concentration normally decreases to its lowest value between 1 and
3 hours after birth, followed by a progressive increase to greater
than 50 to 60 mg/dL by 12 to 24 hours (Fig.
Plasma glucose concentrations during the first week ...
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