Postnatal glucose homeostasis and dysglycemia in newborns: A narrative review

Background: Glucose is the principal substrate for cellular energy production during fetal and neonatal life and is particularly critical for cerebral metabolism. The neonatal brain consumes glucose at a rate disproportionate to body size, rendering newborns especially vulnerable to disturbances in glucose availability. Following birth, the abrupt cessation of placental glucose transfer necessitates rapid metabolic, hormonal, and physiological adaptations to maintain glucose homeostasis. Failure of this adaptive process may result in neonatal hypoglycemia or hyperglycemia, both of which are associated with significant morbidity and potential long-term neurodevelopmental impairment [1, 2]. Objective: To review current evidence regarding postnatal glucose homeostasis in newborns, with emphasis on physiological adaptation after birth, mechanisms underlying neonatal hypoglycemia and hyperglycemia, screening challenges, and clinical consequences. Data Sources: This narrative review is based on peer-reviewed literature cited in a master’s thesis on neonatal glucose homeostasis, including clinical, physiological, and endocrinological studies. Study Selection: English-language articles addressing neonatal glucose physiology, dysglycemia, screening strategies, management approaches, and outcomes were included. Data Extraction: Relevant data were extracted and narratively synthesized, focusing on mechanistic insights and clinical implications rather than quantitative outcomes. Conclusion: Neonatal glucose regulation is a dynamic, developmentally dependent process. Accurate interpretation of blood glucose values requires an understanding of normal physiological adaptation and pathological deviations to prevent adverse neurological outcomes.