Define “brain energy sufficiency” by identifying the key indicators that are altered when levels of adenosine triphosphate and phosphocreatine decrease.
Determine plasma glucose concentrations that adversely affect brain functions under different conditions (eg, SGA, infants of diabetic mothers; neonatal encephalopathy, seizures, sepsis)
Determine brain cellular use of alternate fuels (eg, lactate, ketone bodies), as well as alternate fuel production under conditions of diminished glucose availability with physiological and genetically altered animal models.
Determine the relationship between plasma concentrations of energy substrates on brain structure and function, with such techniques as imaging, mass spectroscopy and 1H, 31P nuclear magnetic resonance spectroscopy; and longitudinal phenotypic evaluations in genetically-modified animal models and in human beings to establish cause-and-effect paradigms.
Determine the biologic basis for regional and cellular vulnerability of the brain during hypoglycemia with the methods noted above, as well as MRI/magnetic resonance spectroscopy along with monitoring of the infant's metabolism.
Determine long-term outcomes in neonates with asymptomatic hypoglycemia, focusing on subtle neurocognitive outcomes including executive functions.
Determine the factors that prevent brain injury from low glucose supply in exclusively breastfed infants and the potential consequences of formula feeding in such infants.
