Perioperative medicine & outcomes

The Association of Fructose Metabolism With Anesthesia/Surgery-Induced Lactate Production

Anesth AnalgPublished Mechanistic study

Main finding · Postoperative serum fructose 1-phosphate (metabolomics)Result — go to the resultMean difference −0.164 ×10 4

Authors' conclusion

These results suggest that anesthesia/surgery activates fructose metabolism, producing excessive lactate in the brain that is associated with postoperative cognitive impairment.

Study context

Population
Patients ≥60 years having surgery under GA; 20-month-old mice exposed to sevoflurane (anesthesia/surgery) or 40% oxygen (control)plus mouse model
Participants
43 patients
Comparison
Delayed neurocognitive recovery (dNCR) vs nondNCR patients; anesthesia/surgery vs control mice
  • dNCRn = 17
Outcome
Postoperative serum fructose 1-phosphate (metabolomics)
Methodological detailsclinical cohort with mouse model, metabolomics, isotope labeling and metabolic flux
  • Clinical cohort with mouse model
  • Metabolomics
  • Isotope labeling and metabolic flux

Main finding

As reported in the abstract

Mean difference

−0.164 ×10 4

P = 0.024

Brain fructose 1-phosphate in mice, mean difference ± 0.555; P = .014
−1.669
Fructose inhibitors reduced increased brain lactate in mice, mean difference ± 4.36, P = .0237
96.0
Fructose inhibitors reduced cognitive dysfunction after anesthesia/surgery in mice, mean difference ± 3.94, P = .0237
69.0

Further findings

OutcomeMean differenceP value
Brain IL-6 in mice (small subsample)Anesthesia/surgery vs Control · ± 3.4488.3P = 0.0237

Brain IL-6 in mice (small subsample)

IL-6 may function upstream in fructose activation

Original publication

The Association of Fructose Metabolism With Anesthesia/Surgery-Induced Lactate Production. Anesth Analg. Published 17 December 2024. doi:10.1213/ane.0000000000007350

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