Fasting prior to transient cerebral ischemia reduces delayed neuronal necrosis

Marie, Christine; Bralet, Anne Marie; Gueldry, Serge; Bralet, J

doi:10.1007/bf01001047

Cited by 61 publications

(43 citation statements)

References 41 publications

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“…Studies also show that fasting protects against ischemia injury in rat brain (Go et al, 1988;Marie et al, 1990), mouse kidney and liver van Ginhoven et al, 2009), and human liver (van Ginhoven et al, 2009). Also, fasting following traumatic brain injury proved to be neuroprotective, resulting in reduced oxidative damage and improved cognitive function (Davis et al, 2008).…”

Section: Starvation and Stress Resistancementioning

confidence: 96%

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

2011

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Section: Starvation and Stress Resistancementioning

confidence: 96%

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

2011

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“…This led the authors to conclude that differences in the ability of the brain to utilize ketones at different developmental stages may influence the protection conferred (Rafiki et al, 2003;Vannucci and Simpson, 2003;Pierre and Pellerin, 2005). In a previous study, a 48-h fast, which results in similar short-term ketosis as that achieved by the ketogenic diet, was found to protect rats against neuronal loss in the striatum, neocortex, and hippocampus produced by 30-min fourvessel occlusion (Marie et al, 1990). There was also a reduction in mortality and the incidence of postischemic seizures in fasted animals.…”

Section: Ischemia and Traumatic Brain Injurymentioning

confidence: 99%

Neuroprotective and disease-modifying effects of the ketogenic diet

Gąsior¹,

Rogawski²,

Hartman³

2006

Behavioural Pharmacology

403

324

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The ketogenic diet has been in clinical use for over 80 years, primarily for the symptomatic treatment of epilepsy. A recent clinical study has raised the possibility that exposure to the ketogenic diet may confer long-lasting therapeutic benefits for patients with epilepsy. Moreover, there is evidence from uncontrolled clinical trials and studies in animal models that the ketogenic diet can provide symptomatic and disease-modifying activity in a broad range of neurodegenerative disorders including Alzheimer's disease and Parkinson's disease, and may also be protective in traumatic brain injury and stroke. These observations are supported by studies in animal models and isolated cells that show that ketone bodies, especially β-hydroxybutyrate, confer neuroprotection against diverse types of cellular injury. This review summarizes the experimental, epidemiological and clinical evidence indicating that the ketogenic diet could have beneficial effects in a broad range of brain disorders characterized by the death of neurons. Although the mechanisms are not yet well defined, it is plausible that neuroprotection results from enhanced neuronal energy reserves, which improve the ability of neurons to resist metabolic challenges, and possibly through other actions including antioxidant and anti-inflammatory effects. As the underlying mechanisms become better understood, it will be possible to develop alternative strategies that produce similar or even improved therapeutic effects without the need for exposure to an unpalatable and unhealthy, high-fat diet.

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“…The exact mechanism of this neuroprotection is still unknown. This study used 31 P nuclear magnetic resonance spectroscopy to monitor energy metabolism during a 3-h episode of HI in 7-d-old rat pups in one of two groups. The first group was pretreated with 0.1 mL saline (i.p.)…”

mentioning

confidence: 99%

Increased Plasma Beta-Hydroxybutyrate, Preserved Cerebral Energy Metabolism, and Amelioration of Brain Damage During Neonatal Hypoxia Ischemia with Dexamethasone Pretreatment

et al. 2000

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Dexamethasone (DEX) pretreatment has been shown to be neuroprotective in a neonatal rat model of hypoxia ischemia (HI). The exact mechanism of this neuroprotection is still unknown. This study used 31 P nuclear magnetic resonance spectroscopy to monitor energy metabolism during a 3-h episode of HI in 7-d-old rat pups in one of two groups. The first group was pretreated with 0.1 mL saline (i.p.) and the second group was treated with 0.1 mL of 0.1mg/kg DEX (i.p.) 22 h before HI. Animals pretreated with DEX had elevated nucleoside triphosphate and phosphocreatine levels during HI when compared with controls. Salinetreated animals had significant decreases in nucleoside triphosphate and phosphocreatine and increases in inorganic phosphate over this same period. 31 P nuclear magnetic resonance data unequivocally demonstrate preservation of energy metabolism during HI in neonatal rats pretreated with DEX. Animals pretreated with DEX had little or no brain damage following 3 h of HI when compared with matched controls, which experienced severe neuronal loss and cortical infarction. These same pretreated animals had an increase in blood beta-hydroxybutyrate levels before ischemia, suggesting an increase in ketone bodies, which is the neonate's primary energy source. Elevation of ketone bodies appears to be one of the mechanisms by which DEX pretreatment provides neuroprotection during HI in the neonatal rat. Abbreviations DEX, dexamethasone HI, hypoxia ischemia NTP, nucleoside triphosphate NMR, nuclear magnetic resonance NMRS, nuclear magnetic resonance spectroscopy BHB, beta-hydroxybutyrate D-␤-HBA, D-␤-hydroxybutyrate dehydrogenase Dexamethasone (DEX) is a synthetic glucocorticoid. A National Institutes of Health consensus committee has recommended its use for women who are believed to deliver prematurely (1). Administered antenatally (before birth), DEX can relieve or ameliorate symptoms associated with respiratory distress syndrome and intraventricular hemorrhage and thus reduce mortality. Research was recommended to guide clinical care on the "effects of antenatal corticosteroids on hypoxic-ischemic insults."The first study to document the effects of DEX on neonatal animals was performed using the modified Levine preparation in neonatal rat by Altman et al. (2). They s.c. injected rat pups with either saline, 4 mg/kg DEX, or 40 mg/kg DEX immediately before hypoxia ischemia (HI). Neither dose of DEX ameliorated brain edema, lactacidemia, or hypoglycemia. In addition, there was no preservation of high-energy metabolites and there was an increase in mortality associated with the highest dose. These negative results made other investigators reluctant to pursue DEX as an effective neuroprotective agent.Barks et al. discovered that pretreatment with DEX 3 h or more before a hypoxic-ischemic insult was neuroprotective (3). DEX at 0.5 mg/kg/d for 3 d, before the insult, prevented brain damage associated with 3 h of cerebral HI in the 7-d-old rat Received August 8, 1998; accepted November 11, 1999

show abstract

Fasting prior to transient cerebral ischemia reduces delayed neuronal necrosis

Cited by 61 publications

References 41 publications

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

Fasting vs dietary restriction in cellular protection and cancer treatment: from model organisms to patients

Neuroprotective and disease-modifying effects of the ketogenic diet

Increased Plasma Beta-Hydroxybutyrate, Preserved Cerebral Energy Metabolism, and Amelioration of Brain Damage During Neonatal Hypoxia Ischemia with Dexamethasone Pretreatment

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