GLUCOSE METABOLISM IN NEWBORN INFANTS WITH CONGENITAL HEART DISEASE

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Sick neonates, including those with congenital heart disease, very often require Total Parenteral Nutrition (TPN) during their first several days of life until their ability to tolerate enteral feeds is well established. These infants, as well as those born prematurely, are at risk of disturbed glucose metabolism and inadequate energy supplementation. In an effort to prevent hypoglycemia and provide a sufficient energy intake, some of these neonates are routinely receiving glucose at rates about twice their normal glucose turn over rate (6 mg/kg/min). This regimen results in a frequent occurrence of hyperglycemia, particularly in premature and sick infants). It has been demonstrated in critically ill children and adults that hyperglycemia was associated with increased mortality (4-5). There are no corresponding studies in newborns, but sick infants also constitute a high risk population. Thus, preventing hyperglycemia, without compromising the energy intake, would most likely reduce their risk of an adverse outcome. There are no published data on the effects of reducing the glucose infusion rate (to prevent or treat hyperglycemia) on glucose metabolism (glucose production, gluconeogenesis and glycogenolysis) in newborns with congenital heart disease. The purpose of this project is to determine the effects of different glucose infusion rates on glucose, lipid, and protein metabolism in newborn infants with congenital heart disease. Knowledge about the physiology of glucose metabolism in these sick neonates is crucial for designing adequate composition of parenteral nutrition that renders them normoglycemic and provide them with a sufficient energy intake.