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ARS Home » Plains Area » Houston, Texas » Children's Nutrition Research Center » Research » Publications at this Location » Publication #138329
Title: GLUCOSE EXTREMES IN NEWBORN INFANTS

Author
item Sunehag, Agneta
item Haymond, Morey

Submitted to: Clinics in Perinatology
Publication Type: Other
Publication Acceptance Date: 5/1/2002
Publication Date: 6/1/2002
Citation: Sunehag AL, Haymond MW. Glucose extremems in newborn infants. 2002 Clin Perinatol 29:245-260.

Interpretive Summary: Glucose is the primary substrate for brain metabolism, and the brain utilizes about 20 times more glucose than muscle and fat. Infants have a large brain to body weight ratio resulting in about three times higher glucose turnover rates on a per kg body weight basis in an infant compared to an adult. Further, 90% of total glucose utilization is by the brain in infants. Following cessation of the transplacental flow of nutrients, most healthy term newborn infants promptly initiate hepatic glucose production to meet their high glucose demands. Most healthy term infants adapt rapidly to the metabolic demands of extrauterine life. However, some infants, although born at term, have disturbed glucose metabolism and are at risk of hypoglycemia (e.g. infants with transient hyperinsulinemia, growth retarded infants (SGA), infants with persistent hyperinsulinemia (PHHI) and with hormone and enzyme defects). We have demonstrated that premature infants born after < 29 weeks of gestation activate their metabolic pathways within the first 24 hours of life and produce glucose at rates comparable to term newborns. Very premature infants, however, have a low tolerance for enteral feeding and they are, therefore, totally dependent on parenteral nutrition during the first weeks of life. However, they have a low tolerance for parenteral glucose resulting in a frequent occurrence of hyperglycemia

Technical Abstract: Most healthy term infants adapt rapidly to the metabolic demands of extrauterine life by activating their glycogenolytic and gluconeogenic pathways within a few hours after birth. Some infants, although born at term, have disturbed glucose metabolism and are at risk of hypoglycemia (e.g. infants with transient hyperinsulinemia, growth retarded infants (SGA), infants with persistent hyperinsulinemia (PHHI) and with hormone and enzyme defects). Premature infants also activate their metabolic pathways shortly after birth, but limited body fuel stores place them at high risk of hypoglycemia. Since these infants have decreased tolerance for enteral feedings, they are dependent on parenteral nutrition during the first week(s) of life. However, they have a low tolerance for parenteral glucose resulting in a frequent occurrence of hyperglycemia.