AI Article Synopsis
- Volatile anesthetics (VAs) are commonly used in medical settings, but their exact mechanisms and potential impacts, particularly on neonatal brain development, are not fully understood.
- In neonatal mice, VAs quickly deplete a key metabolic compound, β-hydroxybutyrate (β-HB), at lower concentrations than needed for anesthesia, while adults show no such depletion.
- The depletion of β-HB in neonates is linked to metabolic processes involving citrate accumulation and changes in fatty acid metabolism, highlighting significant differences in metabolic responses between neonates and adults.
Article Abstract
Volatile anesthetics (VAs) are widely used in medicine, but the mechanisms underlying their effects remain ill-defined. Though routine anesthesia is safe in healthy individuals, instances of sensitivity are well documented, and there has been significant concern regarding the impact of VAs on neonatal brain development. Evidence indicates that VAs have multiple targets, with anesthetic and non-anesthetic effects mediated by neuroreceptors, ion channels, and the mitochondrial electron transport chain. Here, we characterize an unexpected metabolic effect of VAs in neonatal mice. Neonatal blood β-hydroxybutarate (β-HB) is rapidly depleted by VAs at concentrations well below those necessary for anesthesia. β-HB in adults, including animals in dietary ketosis, is unaffected. Depletion of β-HB is mediated by citrate accumulation, malonyl-CoA production by acetyl-CoA carboxylase, and inhibition of fatty acid oxidation. Adults show similar significant changes to citrate and malonyl-CoA, but are insensitive to malonyl-CoA, displaying reduced metabolic flexibility compared to younger animals.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8291971 | PMC |
| http://dx.doi.org/10.7554/eLife.65400 | DOI Listing |
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