3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons

Research output: Contribution to journal › Journal article › Research › peer-review

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3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons. / Marosi, Krisztina; Kim, Sang Woo; Moehl, Keelin; Scheibye-Knudsen, Morten; Cheng, Aiwu; Cutler, Roy; Camandola, Simonetta; Mattson, Mark P.

In: Journal of Neurochemistry, Vol. 139, No. 5, 12.2016, p. 769-781.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Marosi, K, Kim, SW, Moehl, K, Scheibye-Knudsen, M, Cheng, A, Cutler, R, Camandola, S & Mattson, MP 2016, '3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons', Journal of Neurochemistry, vol. 139, no. 5, pp. 769-781. https://doi.org/10.1111/jnc.13868

APA

Marosi, K., Kim, S. W., Moehl, K., Scheibye-Knudsen, M., Cheng, A., Cutler, R., Camandola, S., & Mattson, M. P. (2016). 3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons. Journal of Neurochemistry, 139(5), 769-781. https://doi.org/10.1111/jnc.13868

Vancouver

Marosi K, Kim SW, Moehl K, Scheibye-Knudsen M, Cheng A, Cutler R et al. 3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons. Journal of Neurochemistry. 2016 Dec;139(5):769-781. https://doi.org/10.1111/jnc.13868

Author

Marosi, Krisztina ; Kim, Sang Woo ; Moehl, Keelin ; Scheibye-Knudsen, Morten ; Cheng, Aiwu ; Cutler, Roy ; Camandola, Simonetta ; Mattson, Mark P. / 3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons. In: Journal of Neurochemistry. 2016 ; Vol. 139, No. 5. pp. 769-781.

Bibtex

@article{8866722fd7d14319a71853aa310e76ff,
title = "3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons",
abstract = "During fasting and vigorous exercise, a shift of brain cell energy substrate utilization from glucose to the ketone 3-hydroxybutyrate (3OHB) occurs. Studies have shown that 3OHB can protect neurons against excitotoxicity and oxidative stress, but the underlying mechanisms remain unclear. Neurons maintained in the presence of 3OHB exhibited increased oxygen consumption and ATP production, and an elevated NAD+/NADH ratio. We found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain-derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons. The mechanism by which 3OHB induces Bdnf gene expression involves generation of reactive oxygen species, activation of the transcription factor NF-κB, and activity of the histone acetyltransferase p300/EP300. Because BDNF plays important roles in synaptic plasticity and neuronal stress resistance, our findings suggest cellular signaling mechanisms by which 3OHB may mediate adaptive responses of neurons to fasting, exercise, and ketogenic diets.",
keywords = "bdnf, ketone, mitochondria, nf-kb, p300",
author = "Krisztina Marosi and Kim, {Sang Woo} and Keelin Moehl and Morten Scheibye-Knudsen and Aiwu Cheng and Roy Cutler and Simonetta Camandola and Mattson, {Mark P.}",
year = "2016",
month = dec,
doi = "10.1111/jnc.13868",
language = "English",
volume = "139",
pages = "769--781",
journal = "Journal of Neurochemistry",
issn = "0022-3042",
publisher = "Wiley-Blackwell",
number = "5",

}

RIS

TY - JOUR

T1 - 3-Hydroxybutyrate regulates energy metabolism and induces BDNF expression in cerebral cortical neurons

AU - Marosi, Krisztina

AU - Kim, Sang Woo

AU - Moehl, Keelin

AU - Scheibye-Knudsen, Morten

AU - Cheng, Aiwu

AU - Cutler, Roy

AU - Camandola, Simonetta

AU - Mattson, Mark P.

PY - 2016/12

Y1 - 2016/12

N2 - During fasting and vigorous exercise, a shift of brain cell energy substrate utilization from glucose to the ketone 3-hydroxybutyrate (3OHB) occurs. Studies have shown that 3OHB can protect neurons against excitotoxicity and oxidative stress, but the underlying mechanisms remain unclear. Neurons maintained in the presence of 3OHB exhibited increased oxygen consumption and ATP production, and an elevated NAD+/NADH ratio. We found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain-derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons. The mechanism by which 3OHB induces Bdnf gene expression involves generation of reactive oxygen species, activation of the transcription factor NF-κB, and activity of the histone acetyltransferase p300/EP300. Because BDNF plays important roles in synaptic plasticity and neuronal stress resistance, our findings suggest cellular signaling mechanisms by which 3OHB may mediate adaptive responses of neurons to fasting, exercise, and ketogenic diets.

AB - During fasting and vigorous exercise, a shift of brain cell energy substrate utilization from glucose to the ketone 3-hydroxybutyrate (3OHB) occurs. Studies have shown that 3OHB can protect neurons against excitotoxicity and oxidative stress, but the underlying mechanisms remain unclear. Neurons maintained in the presence of 3OHB exhibited increased oxygen consumption and ATP production, and an elevated NAD+/NADH ratio. We found that 3OHB metabolism increases mitochondrial respiration which drives changes in expression of brain-derived neurotrophic factor (BDNF) in cultured cerebral cortical neurons. The mechanism by which 3OHB induces Bdnf gene expression involves generation of reactive oxygen species, activation of the transcription factor NF-κB, and activity of the histone acetyltransferase p300/EP300. Because BDNF plays important roles in synaptic plasticity and neuronal stress resistance, our findings suggest cellular signaling mechanisms by which 3OHB may mediate adaptive responses of neurons to fasting, exercise, and ketogenic diets.

KW - bdnf

KW - ketone

KW - mitochondria

KW - nf-kb

KW - p300

U2 - 10.1111/jnc.13868

DO - 10.1111/jnc.13868

M3 - Journal article

C2 - 27739595

VL - 139

SP - 769

EP - 781

JO - Journal of Neurochemistry

JF - Journal of Neurochemistry

SN - 0022-3042

IS - 5

ER -

ID: 170736814