Neuroprotection in Diet-Induced Ketotic Rat Brain after Focal Ischemia

[1]  Yong J. Lee,et al.  Flavonoids‐induced accumulation of hypoxia‐inducible factor (HIF)‐1α/2α is mediated through chelation of iron , 2008 .

[2]  M. Prins,et al.  Cerebral Metabolic Adaptation and Ketone Metabolism after Brain Injury , 2008, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[3]  I. Nissim,et al.  The ketogenic diet and brain metabolism of amino acids: relationship to the anticonvulsant effect. , 2007, Annual review of nutrition.

[4]  J. LaManna,et al.  Diet-induced ketosis increases capillary density without altered blood flow in rat brain. , 2007, American journal of physiology. Endocrinology and metabolism.

[5]  J. Rho,et al.  Ketones inhibit mitochondrial production of reactive oxygen species production following glutamate excitotoxicity by increasing NADH oxidation , 2007, Neuroscience.

[6]  K. Petersen,et al.  Measurements of the anaplerotic rate in the human cerebral cortex using 13C magnetic resonance spectroscopy and [1‐13C] and [2‐13C] glucose , 2007, Journal of neurochemistry.

[7]  K. Tsuda Role of hyperglycemia and glutamate receptors in ischemic injury in acute cerebral infarction. , 2006, Stroke.

[8]  J. Krupiński,et al.  Can angiogenesis be exploited to improve stroke outcome? Mechanisms and therapeutic potential. , 2006, Clinical science.

[9]  J. Kelleher,et al.  Metabolomic assays of the concentration and mass isotopomer distribution of gluconeogenic and citric acid cycle intermediates , 2006, Metabolomics.

[10]  A. Nehlig,et al.  Neuronal–glial interactions in rats fed a ketogenic diet , 2006, Neurochemistry International.

[11]  D. MacGrogan,et al.  A ketogenic diet as a potential novel therapeutic intervention in amyotrophic lateral sclerosis , 2006, BMC Neuroscience.

[12]  F. Mochel,et al.  Pyruvate carboxylase deficiency: clinical and biochemical response to anaplerotic diet therapy. , 2005, Molecular genetics and metabolism.

[13]  M. Déry,et al.  Hypoxia-inducible factor 1: regulation by hypoxic and non-hypoxic activators. , 2005, The international journal of biochemistry & cell biology.

[14]  G. Fiskum,et al.  Redox mechanisms of cytoprotection by Bcl-2. , 2005, Antioxidants & redox signaling.

[15]  R. Freeman,et al.  Targeting hypoxia-inducible factor (HIF) as a therapeutic strategy for CNS disorders. , 2005, Current drug targets. CNS and neurological disorders.

[16]  D. Mele,et al.  Therapeutic Effects of l‐Carnitine and Propionyl‐l‐carnitine on Cardiovascular Diseases: A Review , 2004, Annals of the New York Academy of Sciences.

[17]  Till Acker,et al.  Cellular oxygen sensing need in CNS function: physiological and pathological implications , 2004, Journal of Experimental Biology.

[18]  G. Semenza,et al.  Hydroxylation of HIF-1: oxygen sensing at the molecular level. , 2004, Physiology.

[19]  C. Dalgard,et al.  Endogenous 2-oxoacids differentially regulate expression of oxygen sensors. , 2004, The Biochemical journal.

[20]  J. Rho,et al.  The ketogenic diet increases mitochondrial uncoupling protein levels and activity , 2004, Annals of neurology.

[21]  R. Veech The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. , 2004, Prostaglandins, leukotrienes, and essential fatty acids.

[22]  A. Nehlig Brain uptake and metabolism of ketone bodies in animal models. , 2004, Prostaglandins, leukotrienes, and essential fatty acids.

[23]  M. Guzmán,et al.  Ketone body synthesis in the brain: possible neuroprotective effects. , 2004, Prostaglandins, leukotrienes, and essential fatty acids.

[24]  C. Hoppel,et al.  Assessing the Reversibility of the Anaplerotic Reactions of the Propionyl-CoA Pathway in Heart and Liver* , 2003, Journal of Biological Chemistry.

[25]  P. Maher,et al.  The Regulation of Glucose Metabolism by HIF-1 Mediates a Neuroprotective Response to Amyloid Beta Peptide , 2003, Neuron.

[26]  Y. Tsujimoto Cell death regulation by the Bcl‐2 protein family in the mitochondria , 2003 .

[27]  Henri Brunengraber,et al.  Quantitative assessment of anaplerosis from propionate in pig heart in vivo. , 2003, American journal of physiology. Endocrinology and metabolism.

[28]  J. LaManna,et al.  Angiopoietin-2 and rat brain capillary remodeling during adaptation and deadaptation to prolonged mild hypoxia. , 2002, Journal of applied physiology.

[29]  Mark W Parsons,et al.  Acute hyperglycemia adversely affects stroke outcome: A magnetic resonance imaging and spectroscopy study , 2002, Annals of neurology.

[30]  F. Agani,et al.  Role of nitric oxide in the regulation of HIF-1α expression during hypoxia , 2002 .

[31]  R. Ratcheson,et al.  Ischemic Cell Death: Dynamics of Delayed Secondary Energy Failure During Reperfusion Following Focal Ischemia , 2002, Metabolic Brain Disease.

[32]  Takashi Sato,et al.  β-hydroxybutyrate, a cerebral function improving agent, protects rat brain against ischemic damage caused by permanent and transient focal cerebral ischemia , 2002 .

[33]  F. Agani,et al.  Expression of hypoxia-inducible factor-1alpha in the brain of rats during chronic hypoxia. , 2000, Journal of applied physiology.

[34]  K. Clarke,et al.  Erratum: D-β-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease (Proceedings of the National Academy of Sciences of the United States of America (May 9, 2000) 97:10 (5440-5444)) , 2000 .

[35]  K. Clarke,et al.  D-beta-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[36]  J M Freeman,et al.  The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children. , 1998, Pediatrics.

[37]  B. Hassel,et al.  Selective Inhibition of the Tricarboxylic Acid Cycle of GABAergic Neurons with 3‐Nitropropionic Acid In Vivo , 1995, Journal of neurochemistry.

[38]  B. Landau,et al.  R,S-1,3-butanediol acetoacetate esters, potential alternates to lipid emulsions for total parenteral nutrition , 1995 .

[39]  N. Sims,et al.  Delayed treatment with 1,3-butanediol reduces loss of CA1 neurons in the hippocampus of rats following brief forebrain ischemia , 1994, Brain Research.

[40]  F. Sharp,et al.  Infarct Measurement Methodology , 1994, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[41]  L. Rochette,et al.  Beneficial effect of 1,3-butanediol on cerebral energy metabolism and edema following brain embolization in rats. , 1990, Stroke.

[42]  D. Duverger,et al.  The Quantification of Cerebral Infarction following Focal Ischemia in the Rat: Influence of Strain, Arterial Pressure, Blood Glucose Concentration, and Age , 1988, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[43]  K. Kivirikko,et al.  Mechanism of the Prolyl Hydroxylase Reaction , 1982 .

[44]  S. Rapoport,et al.  No Effect of Hyperketonemia on Local Cerebral Glucose Utilization in Conscious Rats , 1982, Journal of neurochemistry.

[45]  K. Kivirikko,et al.  Mechanism of the prolyl hydroxylase reaction. 2. Kinetic analysis of the reaction sequence. , 1977, European journal of biochemistry.

[46]  O. H. Lowry,et al.  Effects of changes in brain metabolism on the levels of citric acid cycle intermediates. , 1966, The Journal of biological chemistry.

[47]  Yong J. Lee,et al.  Flavonoids-induced accumulation of hypoxia-inducible factor (HIF)-1alpha/2alpha is mediated through chelation of iron. , 2008, Journal of cellular biochemistry.

[48]  Eyal Gottlieb,et al.  Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. , 2005, Cancer cell.

[49]  David G. Watson,et al.  Succinate links TCA cycle dysfunction to oncogenesis by inhibiting HIF-alpha prolyl hydroxylase. , 2005, Cancer cell.

[50]  Kazunori Sato,et al.  Beta-hydroxybutyrate, a cerebral function improving agent, protects rat brain against ischemic damage caused by permanent and transient focal cerebral ischemia. , 2002, Japanese journal of pharmacology.