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DEFICIENT KETOGENESIS IN NEONATAL HYPOGLYCEMIA

To investigate the reasons for the high incidence of neonatal hypoglycemia, hormone and metabolic fuel responses to postnatal fasting were examined in 24 term-AGA, 9 preterm-AGA, 6 term-SGA, and 4 preterm-SGA infants. At 8 hours of age or when plasma glucose (GLU) was <40mg%, blood was drawn for determinations of GLU, gluconeogenic substrates, fat-derived fuels, and hormones. Fuel and hormone levels in the preterm-AGA and 2 SGA groups were similar to term-AGA infants: lactate 2.9±.22mM (m±SEM), pyruvate .16±.01mM; alanine .48±.02mM; free fatty acids 1.4±.07mM: b-OH-butyrate .32±.04mM; acetoacetate .05±.01mM; insulin 10±9uU/ml: growth hormone 16±3ng/ml; cortisol 8±1.3ug/dl. Asymptomatic hypoglycemia (GLU ≤ 40mg%) occurred in 18% of AGA and 80% of SGA infants. In the 14 hypoglycemic infants, ketone levels were low (b-OH-butyrate .21±.04mM) despite low insulin (8±1.3uU/ml) and high free fatty acid levels (1.2±.14mM).These results suggest that capacity for hepatic ketogenesis is low during postnatal fasting. This may be a primary factor limiting the ability of neonates to tolerate fasting. In addition, at times of hypoglycemia, ketones are not available as fuel for CNS metabolism. This raises concerns about whether the currently accepted definition of hypoglycemia in the neonatal period provides sufficient margin for safety.