Closing the gap before using L-lactate to guide newborn care

Abstract

We thank the authors for their insightful commentary on our study investigating sodium L-lactate (NaL) supplementation in preterm infants with metabolic acidosis. Their analysis highlights lactate's expanding role beyond a metabolic byproduct, emphasizing its functions in cellular signaling, antioxidant defense, and neuroprotection. Our study demonstrated that NaL improved acid-base balance without adverse effects, likely through lactate's conversion to bicarbonate and potential support for mitochondrial function. The commentary further explores NaL's translational relevance in neonatal hypoxia-ischemia (NHI), where lactate may serve as a key neuroenergetic substrate and modulate inflammation and gene expression. While the Rice-Vannucci model has limitations, it remains valuable for long-term studies, as shown in our prior work. We agree that larger animal models offer enhanced physiological relevance but face practical constraints. Future research should compare NaL with sodium acetate (NaA), a standard in neonatal care, to assess relative benefits in correcting acidosis and supporting neurodevelopment. We support the call for randomized, multicenter studies with long-term follow-up to fully evaluate NaL's therapeutic potential in preterm and at-risk neonates. IMPACT: L-lactate is a key component of the astrocyte-neuron lactate shuttle, supporting brain energy metabolism. Ibrahim et al. suggest sodium L-lactate as an alternative maintenance fluid for preterm newborns. L-lactate should not be regarded merely as a simple fluid replacement. L-lactate acts as a signaling molecule, impacting cellular metabolism and brain development. Additional research is required to assess the potential benefits and safety of sodium L-lactate in newborns.