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Lactate, glucose and the neonatal brain: it’s time to challenge the paradigm
  1. Martin Ward Platt
  1. Correspondence to Dr Martin Ward Platt, Neonatal Service (Ward 35), Royal Victoria Infirmary, Queen Victoria Road, Newcastle upon Tyne NE1 4LP, UK; m.p.ward-platt{at}ncl.ac.uk

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The association in clinicians’ minds between lactate and hypoxia, and lactate and acidosis, has cast this small, innocent three-carbon molecule in the role of bad boy: a demonised hoody rather than a helpful little fuel. That this ‘bad boy’ role is a misconception has been known for many years, but known more by the cognoscenti of intermediary metabolism rather than working clinicians. The companion paper by Harris et al1 will help to redress the balance: it provides useful additional information about the role of lactate when babies become hypoglycaemic, and these new data reinforce its importance as a metabolic fuel. In case you missed it, this was also emphasised in a recent article in our Education and Practice edition.2

In considering the mechanisms of glucose homoeostasis in the neonate, it is important to distinguish the mechanisms by which healthy babies remain healthy, and the way that babies cope when normal adaptive mechanisms fail, and threaten to make them unhealthy. Most knowledge of the biochemical physiology of fuel metabolism in the newborn has been obtained using fuel turnover studies in healthy babies in, or close to, metabolic steady state, but the reality for babies becoming hypoglycaemic is that their state is anything but steady, and the mechanisms they …

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