Ketone Bodies after Cardiac Arrest: A Narrative Review and the Rationale for Use.
Filippo AnnoniElisa Gouvea BogossianLorenzo PelusoFuhong SuAnthony MoreauLeda NobileStefano Giuseppe CasuElda Diletta StercheleLorenzo CalabroMichele SalvagnoMauro OddoFabio Silvio TacconePublished in: Cells (2024)
Cardiac arrest survivors suffer the repercussions of anoxic brain injury, a critical factor influencing long-term prognosis. This injury is characterised by profound and enduring metabolic impairment. Ketone bodies, an alternative energetic resource in physiological states such as exercise, fasting, and extended starvation, are avidly taken up and used by the brain. Both the ketogenic diet and exogenous ketone supplementation have been associated with neuroprotective effects across a spectrum of conditions. These include refractory epilepsy, neurodegenerative disorders, cognitive impairment, focal cerebral ischemia, and traumatic brain injuries. Beyond this, ketone bodies possess a plethora of attributes that appear to be particularly favourable after cardiac arrest. These encompass anti-inflammatory effects, the attenuation of oxidative stress, the improvement of mitochondrial function, a glucose-sparing effect, and the enhancement of cardiac function. The aim of this manuscript is to appraise pertinent scientific literature on the topic through a narrative review. We aim to encapsulate the existing evidence and underscore the potential therapeutic value of ketone bodies in the context of cardiac arrest to provide a rationale for their use in forthcoming translational research efforts.
Keyphrases
- cardiac arrest
- cerebral ischemia
- brain injury
- subarachnoid hemorrhage
- cardiopulmonary resuscitation
- blood brain barrier
- cognitive impairment
- oxidative stress
- physical activity
- white matter
- clinical trial
- blood glucose
- spinal cord injury
- weight loss
- young adults
- metabolic syndrome
- high intensity
- resting state
- insulin resistance
- dna damage
- ischemia reperfusion injury
- type diabetes
- signaling pathway
- endoplasmic reticulum stress
- multiple sclerosis
- diabetic rats