Abstract 1992 Metabolic Deficiencies Inhibit Angiogenic Properties and Vascular Well-being in a Hyperoxic Environment

Metabolic pathways and their functional consequences on lung alveolar formation and vascular dysfunction in premature infants are poorly understood. Misalignment of infants' metabolic demands with nutrient availability have a prolonged and profound impact on infant growth. Nicotinamide adenine dinucleotide (NAD+), a regulator of the cellular stress response and neovascularization in pathologic disease processes, is insufficient in preterm infants. NAD+ levels are dependent on dietary intake of B3 vitamin, Nicotinamide (NAM).