The evolutionary loss of the main enzyme required for ketone body biosynthesis suggests that alternative strategies to provide energy for large brains during fasting evolved repeatedly in mammals.

Exposure to ketone bodies in early development can reduce neurological impairments in a strain of the nematode C. elegans with PTEN defects.

Glucocorticoid receptor directly regulates the transcriptional activity of peroxisome proliferator-activated alpha (PPARα) before birth in anticipation of the sudden shifts in the postnatal nutrient source and metabolic demands.

Acetate concentration, which is significantly increased in association with energy stresses such as those that occur with diabetes or starvation, is emerging as a novel 'ketone body' with potential as a parameter for evaluating the progression of energy stress.

PTEN mutations disrupt inhibitory GABAergic signaling, causing neurodevelopmental defects that can be mitigated by β-hydroxybutyrate, which activates DAF-16/FOXO and may offer a therapeutic approach for excitation/inhibition imbalances.

Glutamatergic neurons lacking the mitochondrial pyruvate carrier show reduced M-type potassium channel activity and hyperexcitability upon intense firing.

Volatile anesthetics impair hepatic tricarboxylic acid cycle function in adult and neonatal mice, with citrate accumulation driving a neonate-specific inhibition of beta-oxidation and ketosis through their increased relative sensitivity to malonyl-CoA.

β-Hydroxybutyrate accumulates in the perfused rat heart during ischaemia, driven by flux through both HMGCS and SCOT, with implications for functional recovery.

A potential link between metabolic changes resulting from exercise and gene expression in the brain has been revealed.

Elephants and fruit bats have evolved large brains even though they have lost a gene that is fundamental to the supply of energy to the brain when glucose is not available.