KETOGENIC DIET | Dietary Management of Epilepsy: Role of Glucose and Ketone Bodies

2009 ◽  
pp. 687-693 ◽  
Author(s):  
T.N. Seyfried ◽  
J.G. Mantis ◽  
M.T. Todorova ◽  
A.E. Greene
Keyword(s):  
Ketogenic Diet ◽  
Ketone Bodies ◽  
Dietary Management

Ketogenic Diet and PPARgamma

2016 ◽  
Author(s):  
Timothy A. Simeone
Keyword(s):  
Ketogenic Diet ◽  
Refractory Epilepsy ◽  
Ketone Bodies ◽  
Peroxisome Proliferator ◽  
Potential Therapeutic Target ◽  
Peroxisome Proliferator Activated Receptor ◽  
Nuclear Transcription Factor ◽  
Inflammatory Processes ◽  
The Brain

The ketogenic diet (KD) is an effective therapy for many patients with refractory epilepsy. It engages a wide array of antioxidant and anti-inflammatory processes and improves mitochondrial function, which is thought to underlie its neuroprotective, antiseizure, and disease-modifying effects. Potential roles of ketone bodies in these mechanisms are discussed elsewhere in this volume. This chapter focuses on the role of KD fatty acids as potential ligands for the nutritionally regulated nuclear transcription factor peroxisome proliferator activated receptor gamma (PPARgamma). PPARgamma regulates many of the pathways identified in the mechanism of the KD and, in recent years, has become a potential therapeutic target for neurodegenerative diseases. This chapter reviews what is known concerning PPARgamma in the brain, the evidence that PPARgamma has neuroprotective and antiseizure properties, and the evidence suggesting that PPARgamma may be involved in the antiseizure mechanisms of the ketogenic diet.

Dietetic approaches to organisation of a ketogenic diet in children with epilepsy

2020 ◽  
Vol 18 (6) ◽  
pp. 35-40
Author(s):  
E.A. Pyrieva ◽  
◽  
A.I. Safronova ◽  
M.A. Toboleva ◽  
K.V. Osipova ◽  
...  
Keyword(s):  
Ketogenic Diet ◽  
Ketone Bodies ◽  
Diet Therapy ◽  
Medium Chain Triglycerides ◽  
Considerable Decrease ◽  
Pharmacoresistant Epilepsy ◽  
Calcium Phosphorus ◽  
Modified Diet ◽  
Methods Of Control

The article presents current dietetic approaches to organisation of a ketogenic diet (KD) in children with pharmacoresistant epilepsy. The indications, contraindications, side effects of KD are considered as well as methods of control over patients who receive ketogenic diet therapy, information recourses for it’s application are provided. Characteristics of KDs used in epilepsy are given – the classical, MCT, the Atkins modified diet, and a low-glycemic diet. The role of specialised food products designed for patients who need a ketogenic diet is outlined. The results of studying the actual nutrition of children with pharmacoresistant epilepsy who receive KD are indicative of a considerable decrease, as compared with the recommended allowances, of the levels of vitamins (С, В1, В2, folates, D3) and mineral substances (calcium, phosphorus, magnesium, iron, selenium). The results demonstrate good prospects for a broader application of KD in clinical practice with collaboration of neurologists and dietitians. Key words: children, ketogenic diet, ketone bodies, medium-chain triglycerides, epilepsy

scholarly journals Glioblastoma utilizes fatty acids and ketone bodies for growth allowing progression during ketogenic diet therapy

2019 ◽  
Author(s):  
Jantzen Sperry ◽  
Michael C. Condro ◽  
Lea Guo ◽  
Daniel Braas ◽  
Nathan Vanderveer-Harris ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Ketogenic Diet ◽  
Ketone Bodies ◽  
Aerobic Glycolysis ◽  
Diet Therapy ◽  
Acid Oxidation ◽  
Reduce Tumor Growth

SummaryGlioblastoma (GBM) metabolism has traditionally been characterized by a primary dependence on aerobic glycolysis, prompting the use of the ketogenic diet (KD) as a potential therapy. In this study we evaluated the effectiveness of the KD in GBM and assessed the role of fatty acid oxidation (FAO) in promoting GBM propagation. In vitro assays revealed FA utilization throughout the GBM metabolome, and growth inhibition in nearly every cell line in a broad spectrum of patient-derived glioma cells treated with FAO inhibitors. In vivo assessments revealed that knockdown of carnitine palmitoyltransferase 1A (CPT1A), the rate limiting enzyme for FAO, reduced the rate of tumor growth and increased survival. However, the unrestricted ketogenic diet did not reduce tumor growth, and for some models significantly reduced survival. Altogether, these data highlight important roles for FA and ketone body metabolism that could serve to improve targeted therapies in GBM.

Possible Role of High-Dose Barbiturates and Early Administration of Parenteral Ketogenic Diet for Reducing Development of Chronic Epilepsy in Febrile Infection-Related Epilepsy Syndrome: A Case Report

2020 ◽  
Author(s):  
Shimpei Baba ◽  
Tohru Okanishi ◽  
Koichi Ohsugi ◽  
Rika Suzumura ◽  
Keiko Niimi ◽  
...  
Keyword(s):  
Continuous Infusion ◽  
Ketogenic Diet ◽  
Epilepsy Syndrome ◽  
High Dose ◽  
Early Administration ◽  
Chronic Epilepsy ◽  
Time Period ◽  
Irreversible Brain Damage ◽  
Electroencephalogram Eeg

AbstractWe describe the efficacy of high-dose barbiturates and early administration of a parenteral ketogenic diet (KD) as initial treatments for acute status epilepticus (SE) in an 8-year-old girl with febrile infection-related epilepsy syndrome (FIRES). The patient was admitted to our hospital with refractory focal SE. Abundant epileptic discharges over the left frontal region were observed on electroencephalogram (EEG). Treatment with continuous infusion of thiamylal for 4 hours, increased incrementally to 40 mg/kg/h, successfully ended the clinical SE, and induced a burst-suppression coma. The infusion rate was then gradually decreased to 4 mg/kg/h over the next 12 hours. Parenteral KD was administered from days 6 to 21 of illness. Continuous infusion of thiamylal was switched to midazolam on day 10 without causing seizures or EEG exacerbations. The patient has remained seizure free in the 15 months since hospital discharge. The effectiveness of KD for the treatment of FIRES has attracted attention amongst clinicians, but KD treatment may need to last for 2 to 4 days before it can stop SE, a time period that could cause irreversible brain damage. Considering the severity of SE in our patient and the dose of barbiturates needed to treat it, we consider this case to have had a good clinical outcome. The results suggest that rapid termination of seizure using high-dose barbiturates in conjunction with early administration of parenteral KD could reduce the development of chronic epilepsy in patients with FIRES.

Role of dietary management in children with intestinal failure

2008 ◽  
Vol 40 (10) ◽  
pp. A115
Author(s):  
M.P. Cicalese ◽  
B. Aceto ◽  
A.L. Nappi ◽  
A.M. Salzano ◽  
F. Marciano ◽  
...  
Keyword(s):  
Intestinal Failure ◽  
Dietary Management

scholarly journals The ketogenic diet increases Neuregulin 1 expression via elevating histone acetylation and its anti-seizure effect requires ErbB4 kinase activity

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Jin Wang ◽  
Jie Huang ◽  
Shan Yao ◽  
Jia-Hui Wu ◽  
Hui-Bin Li ◽  
...  
Keyword(s):  
Histone Acetylation ◽  
Ketogenic Diet ◽  
Chromatin Immunoprecipitation ◽  
Kinase Activity ◽  
Control Diet ◽  
Synaptic Activity ◽  
Therapeutic Interventions ◽  
Type I ◽  
Neuregulin 1

Abstract Background The ketogenic diet (KD)has been considered an effective treatment for epilepsy, whereas its underlying mechanisms remain obscure. We have previously reported that the KD feeding increased Neuregulin 1 (NRG1) expression in the hippocampus; disruption of NRG1 signaling by genetically deleting its receptor-ErbB4 abolished KD’s effects on inhibitory synaptic activity and seizures. However, it is still unclear about the mechanisms underlying the effect of KD on NRG1 expression and whether the effects of KD require ErbB4 kinase activity. Methods The effects of the KD on NRG1 expression were assessed via western blotting and real-time PCR. Acetylation level at the Nrg1 promoter locus was examined using the chromatin immunoprecipitation technique. Kainic acid (KA)-induced acute seizure model was utilized to examine the effects of KD and histone deacetylase inhibitor-TSA on seizures. Synaptic activities in the hippocampus were recorded with the technique of electrophysiology. The obligatory role of ErbB4 kinase activity in KD’s effects on seizures and inhibitory synaptic activity was evaluated by using ErbB kinase antagonist and transgenic mouse-T796G. Results We report that KD specifically increases Type I NRG1 expression in the hippocampus. Using the chromatin immunoprecipitation technique, we observe increased acetylated-histone occupancy at the Nrg1 promoter locus of KD-fed mice. Treatment of TSA dramatically elevates NRG1 expression and diminishes the difference between the effects of the control diet (CD) and KD. These data indicate that KD increases NRG1 expression via up-regulating histone acetylation. Moreover, both pharmacological and genetic inhibitions of ErbB4 kinase activity significantly block the KD’s effects on inhibitory synaptic activity and seizure, suggesting an essential role of ErbB4 kinase activity. Conclusion These results strengthen our understanding of the role of NRG1/ErbB4 signaling in KD and shed light on novel therapeutic interventions for epilepsy.

Prognostic factors of infantile spasms: Role of treatment options including a ketogenic diet

2013 ◽  
Vol 35 (8) ◽  
pp. 821-826 ◽  
Author(s):  
Jeehun Lee ◽  
Jun Hwa Lee ◽  
Hee Jun Yu ◽  
Munhyang Lee
Keyword(s):  
Prognostic Factors ◽  
Ketogenic Diet ◽  
Treatment Options ◽  
Infantile Spasms

scholarly journals Possible Clues for Brain Energy Translation via Endolysosomal Trafficking of APP-CTFs in Alzheimer’s Disease

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Senthilkumar Sivanesan ◽  
Ravi Mundugaru ◽  
Jayakumar Rajadas
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Ketone Bodies ◽  
Brain Regions ◽  
Pentose Phosphate ◽  
Lactate Shuttle ◽  
Carboxy Terminal ◽  
Brain Energy

Vascular dysfunctions, hypometabolism, and insulin resistance are high and early risk factors for Alzheimer’s disease (AD), a leading neurological disease associated with memory decline and cognitive dysfunctions. Early defects in glucose transporters and glycolysis occur during the course of AD progression. Hypometabolism begins well before the onset of early AD symptoms; this timing implicates the vulnerability of hypometabolic brain regions to beta-secretase 1 (BACE-1) upregulation, oxidative stress, inflammation, synaptic failure, and cell death. Despite the fact that ketone bodies, astrocyte-neuron lactate shuttle, pentose phosphate pathway (PPP), and glycogenolysis compensate to provide energy to the starving AD brain, a considerable energy crisis still persists and increases during disease progression. Studies that track brain energy metabolism in humans, animal models of AD, and in vitro studies reveal striking upregulation of beta-amyloid precursor protein (β-APP) and carboxy-terminal fragments (CTFs). Currently, the precise role of CTFs is unclear, but evidence supports increased endosomal-lysosomal trafficking of β-APP and CTFs through autophagy through a vague mechanism. While intracellular accumulation of Aβ is attributed as both the cause and consequence of a defective endolysosomal-autophagic system, much remains to be explored about the other β-APP cleavage products. Many recent works report altered amino acid catabolism and expression of several urea cycle enzymes in AD brains, but the precise cause for this dysregulation is not fully explained. In this paper, we try to connect the role of CTFs in the energy translation process in AD brain based on recent findings.

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