The effect of ketogenic diet on behaviors and synaptic functions of naive mice

Huang, Jie; Li, Yuanquan; Wu, Chunqing; Zhang, Yun-Long; Zhao, Shuoxian; Chen, Yongjun; Deng, Yuhong; Xuan, Aiguo; Sun, Xiangdong

doi:10.1002/brb3.1246

Cited by 23 publications

(23 citation statements)

References 55 publications

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“…In the study by Zhang et al (2018a, b), NAA, Cho, CR contents were assessed with MRI spectroscopy in animals fed a ketogenic diet after TBI. In addition, studies by Huang et al (2019) showed that KD applied for 3 months in mice did not cause changes in behavior when tested. But when the threshold for pentylenetetrazole-induced seizures was tested, it turned out to be higher in animals on KD.…”

Section: Introductionmentioning

confidence: 99%

MRI spectroscopic and tractography studies indicate consequences of long-term ketogenic diet

Gzieło¹,

Janeczko²,

Węglarz

et al. 2020

Brain Struct Funct

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To maintain its functional abilities, the mature brain obtains energy from glucose produced in carbohydrate metabolism. When carbohydrates are eliminated from the diet, the energy comes from the oxidation of fatty acids. In this metabolic state called ketosis, ketone bodies are formed: β-hydroxybutyric acid (bHb), acetone, and acetoacetate as alternative source of energy passing through the blood-brain barrier easily. The ketosis state can be achieved through various strategies like caloric restriction, supplementation with medium-chain triglycerides, intense physical training, or ketogenic diet (KD). Using KD, drug-resistant epilepsy has been successfully treated in children and adults. It can also exert neuroprotective influences in cases of brain damage, glioblastoma multiforme, and Alzheimer's or Parkinson's diseases. Although many possible mechanisms of KD activity have been proposed, newer hypotheses appear with the research progress, mostly characterizing the brain under pathological but not normal conditions. Since different pathological conditions may affect the mechanism of KD action differently, additional research on the normal brain appears reasonable. For this purpose, young adult rats were treated with 4-month-lasting KD. Then, MRI structural measurements, spectroscopy, and tractography were performed. The procedures revealed significant increases in the concentration of glutamine, glutamate, glutathione and NAA, accompanied by changes in the pattern of neuronal connections of the striatum and hippocampal formation. This implies a possible involvement of these structures in the functional changes occurring in the brain after KD application. Thus, the investigations on the normal brain add important details concerning mechanisms underlying KD effects without their possible modification by a pathological status.

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Section: Introductionmentioning

confidence: 99%

MRI spectroscopic and tractography studies indicate consequences of long-term ketogenic diet

Gzieło¹,

Janeczko²,

Węglarz

et al. 2020

Brain Struct Funct

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“…Cortical excitability was described as improved due to a reduction in long-term potentiation, without any change in baseline excitability or impact on normal brain activity. Not all studies noted reduced long-term potentiation (67) . 14.…”

Section: Alterations In Cellular Energetics and Metabolismmentioning

confidence: 99%

Ketogenic diets and the nervous system: a scoping review of neurological outcomes from nutritional ketosis in animal studies

Field

Pourkazemi

et al. 2021

Nutr. Res. Rev.

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Objectives: Ketogenic diets have reported efficacy for neurological dysfunctions however there are limited published human clinical trials elucidating the mechanisms by which nutritional ketosis produces therapeutic effects. The purpose of this present study was to investigate animal models that report variations in nervous system function by changing from a standard animal diet to a ketogenic diet, synthesise these into broad themes, and compare these with mechanisms reported as targets in pain neuroscience to inform human chronic pain trials. Methods: An electronic search of seven databases was conducted in July 2020. Two independent reviewers screened studies for eligibility, and descriptive outcomes relating to nervous system function were extracted for a thematic analysis then synthesised into broad themes. Results: One hundred and seventy studies from 18 different disease models were identified and grouped into 14 broad themes including: alterations in cellular energetics and metabolism, biochemical, cortical excitability, epigenetic regulation, mitochondrial function, neuroinflammation, neuroplasticity, neuroprotection, neurotransmitter function, nociception, redox balance, signalling pathways, synaptic transmission and vascular supply. Discussion: The mechanisms presented centred around the reduction of inflammation and oxidative stress as well as a reduction in nervous system excitability. Given the multiple potential mechanisms presented, it is likely that many of these are involved synergistically and undergo adaptive processes within the human body, and controlled animal models that limit the investigation to a particular pathway in isolation may reach differing conclusions. Attention is required when translating this information to human chronic pain populations due to the limitation outlined from the animal research.

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“…Diets were purchased from Research Diets, Inc (New Brunswick, NJ, USA). The control diet consisted of 10% protein, 80% carbohydrates and 10% fat, whereas ketogenic diet consisted of 10% protein and 90% fat [17]. All procedures involving animals were performed in accordance with protocols approved by Rutgers Biomedical and Health Sciences (Protocol Number: 999900700).…”

Section: Ketogenic Dietmentioning

confidence: 99%

β-Hydroxybutyrate, a Ketone Body, Potentiates the Antioxidant Defense via Thioredoxin 1 Upregulation in Cardiomyocytes

et al. 2021

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Thioredoxin 1 (Trx1) is a major antioxidant that acts adaptively to protect the heart during the development of diabetic cardiomyopathy. The molecular mechanism(s) responsible for regulating the Trx1 level and/or activity during diabetic cardiomyopathy is unknown. β-hydroxybutyrate (βHB), a major ketone body in mammals, acts as an alternative energy source in cardiomyocytes under stress, but it also appears to be involved in additional mechanisms that protect the heart against stress. βHB upregulated Trx1 in primary cultured cardiomyocytes in a dose- and a time-dependent manner and a ketogenic diet upregulated Trx1 in the heart. βHB protected cardiomyocytes against H2O2-induced death, an effect that was abolished in the presence of Trx1 knockdown. βHB also alleviated the H2O2-induced inhibition of mTOR and AMPK, known targets of Trx1, in a Trx1-dependent manner, suggesting that βHB potentiates Trx1 function. It has been shown that βHB is a natural inhibitor of HDAC1 and knockdown of HDAC1 upregulated Trx1 in cardiomyocytes, suggesting that βHB may upregulate Trx1 through HDAC inhibition. βHB induced Trx1 acetylation and inhibited Trx1 degradation, suggesting that βHB-induced inhibition of HDAC1 may stabilize Trx1 through protein acetylation. These results suggest that βHB potentiates the antioxidant defense in cardiomyocytes through the inhibition of HDAC1 and the increased acetylation and consequent stabilization of Trx1. Thus, modest upregulation of ketone bodies in diabetic hearts may protect the heart through the upregulation of Trx1.

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The effect of ketogenic diet on behaviors and synaptic functions of naive mice

Cited by 23 publications

References 55 publications

MRI spectroscopic and tractography studies indicate consequences of long-term ketogenic diet

MRI spectroscopic and tractography studies indicate consequences of long-term ketogenic diet

Ketogenic diets and the nervous system: a scoping review of neurological outcomes from nutritional ketosis in animal studies

β-Hydroxybutyrate, a Ketone Body, Potentiates the Antioxidant Defense via Thioredoxin 1 Upregulation in Cardiomyocytes

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