Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner

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Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner. / Zarnowski, Tomasz; Choragiewicz, Tomasz J; Schuettauf, Frank; Zrenner, Eberhart; Rejdak, Robert; Gasior, Maciej; Zarnowska, Iwona; Thaler, Sebastian.

in: OPHTHALMIC RES, Jahrgang 53, Nr. 3, 2015, S. 162-7.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

Harvard

Zarnowski, T, Choragiewicz, TJ, Schuettauf, F, Zrenner, E, Rejdak, R, Gasior, M, Zarnowska, I & Thaler, S 2015, 'Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner', OPHTHALMIC RES, Jg. 53, Nr. 3, S. 162-7. https://doi.org/10.1159/000379753

APA

Zarnowski, T., Choragiewicz, T. J., Schuettauf, F., Zrenner, E., Rejdak, R., Gasior, M., Zarnowska, I., & Thaler, S. (2015). Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner. OPHTHALMIC RES, 53(3), 162-7. https://doi.org/10.1159/000379753

Vancouver

Bibtex

@article{d4b6ba33d8c342b0b092a2dd7c169459,
title = "Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner",
abstract = "OBJECTIVE: This study was conducted to investigate neuroprotective effects of a high fat/low carbohydrate and protein diet (ketogenic diet, KD) in a model of N-methyl D-aspartate (NMDA)-induced retinal ganglion cell (RGC) damage in juvenile and young adult rats.METHODS: Juvenile (30-35 days old) and young adult (56-70 days old) female Brown Norway rats were fed the KD for 21 days; rats exposed to a standard rodent diet (SRD) served as controls. The main constituents of the KD used in the present study were approximately 80% fats, 8% proteins, and less than 1% carbohydrates. On day 14 of exposure to the KD (or the SRD in the control group), each rat received a single intravitreal injection of NMDA; RGCs were then retrogradely labelled by hydroxystilbamidine on day 19 and collected on day 21 to assess the degree of damage induced by NMDA. Blood biomarkers to confirm the expected metabolic response to the KD (i.e. ketosis and hypoglycaemia) were also assessed.RESULTS: Although both the juvenile and young adult rats developed comparable ketosis and hypoglycaemia when fed the KD, NMDA-induced loss in RGCs was significantly attenuated only in juvenile rats exposed to the KD in comparison with those fed the SRD; exposure to the KD had no protective effect in young adult rats. In summary, exposure to the KD had a neuroprotective effect in NMDA-induced RGC damage in juvenile rats, but not in young adult rats.CONCLUSION: These results support further exploration of metabolic interventions to treat optic neuropathies associated with neurodegeneration.",
keywords = "Animals, Cell Count, D-Aspartic Acid/metabolism, Diet Therapy/methods, Diet, Ketogenic, Disease Models, Animal, Female, N-Methylaspartate/toxicity, Neuroprotective Agents/administration & dosage, Rats, Rats, Inbred BN, Retinal Degeneration/chemically induced, Retinal Ganglion Cells/cytology",
author = "Tomasz Zarnowski and Choragiewicz, {Tomasz J} and Frank Schuettauf and Eberhart Zrenner and Robert Rejdak and Maciej Gasior and Iwona Zarnowska and Sebastian Thaler",
note = "{\textcopyright} 2015 S. Karger AG, Basel.",
year = "2015",
doi = "10.1159/000379753",
language = "English",
volume = "53",
pages = "162--7",
journal = "OPHTHALMIC RES",
issn = "0030-3747",
publisher = "S. Karger AG",
number = "3",

}

RIS

TY - JOUR

T1 - Ketogenic diet attenuates NMDA-induced damage to rat's retinal ganglion cells in an age-dependent manner

AU - Zarnowski, Tomasz

AU - Choragiewicz, Tomasz J

AU - Schuettauf, Frank

AU - Zrenner, Eberhart

AU - Rejdak, Robert

AU - Gasior, Maciej

AU - Zarnowska, Iwona

AU - Thaler, Sebastian

N1 - © 2015 S. Karger AG, Basel.

PY - 2015

Y1 - 2015

N2 - OBJECTIVE: This study was conducted to investigate neuroprotective effects of a high fat/low carbohydrate and protein diet (ketogenic diet, KD) in a model of N-methyl D-aspartate (NMDA)-induced retinal ganglion cell (RGC) damage in juvenile and young adult rats.METHODS: Juvenile (30-35 days old) and young adult (56-70 days old) female Brown Norway rats were fed the KD for 21 days; rats exposed to a standard rodent diet (SRD) served as controls. The main constituents of the KD used in the present study were approximately 80% fats, 8% proteins, and less than 1% carbohydrates. On day 14 of exposure to the KD (or the SRD in the control group), each rat received a single intravitreal injection of NMDA; RGCs were then retrogradely labelled by hydroxystilbamidine on day 19 and collected on day 21 to assess the degree of damage induced by NMDA. Blood biomarkers to confirm the expected metabolic response to the KD (i.e. ketosis and hypoglycaemia) were also assessed.RESULTS: Although both the juvenile and young adult rats developed comparable ketosis and hypoglycaemia when fed the KD, NMDA-induced loss in RGCs was significantly attenuated only in juvenile rats exposed to the KD in comparison with those fed the SRD; exposure to the KD had no protective effect in young adult rats. In summary, exposure to the KD had a neuroprotective effect in NMDA-induced RGC damage in juvenile rats, but not in young adult rats.CONCLUSION: These results support further exploration of metabolic interventions to treat optic neuropathies associated with neurodegeneration.

AB - OBJECTIVE: This study was conducted to investigate neuroprotective effects of a high fat/low carbohydrate and protein diet (ketogenic diet, KD) in a model of N-methyl D-aspartate (NMDA)-induced retinal ganglion cell (RGC) damage in juvenile and young adult rats.METHODS: Juvenile (30-35 days old) and young adult (56-70 days old) female Brown Norway rats were fed the KD for 21 days; rats exposed to a standard rodent diet (SRD) served as controls. The main constituents of the KD used in the present study were approximately 80% fats, 8% proteins, and less than 1% carbohydrates. On day 14 of exposure to the KD (or the SRD in the control group), each rat received a single intravitreal injection of NMDA; RGCs were then retrogradely labelled by hydroxystilbamidine on day 19 and collected on day 21 to assess the degree of damage induced by NMDA. Blood biomarkers to confirm the expected metabolic response to the KD (i.e. ketosis and hypoglycaemia) were also assessed.RESULTS: Although both the juvenile and young adult rats developed comparable ketosis and hypoglycaemia when fed the KD, NMDA-induced loss in RGCs was significantly attenuated only in juvenile rats exposed to the KD in comparison with those fed the SRD; exposure to the KD had no protective effect in young adult rats. In summary, exposure to the KD had a neuroprotective effect in NMDA-induced RGC damage in juvenile rats, but not in young adult rats.CONCLUSION: These results support further exploration of metabolic interventions to treat optic neuropathies associated with neurodegeneration.

KW - Animals

KW - Cell Count

KW - D-Aspartic Acid/metabolism

KW - Diet Therapy/methods

KW - Diet, Ketogenic

KW - Disease Models, Animal

KW - Female

KW - N-Methylaspartate/toxicity

KW - Neuroprotective Agents/administration & dosage

KW - Rats

KW - Rats, Inbred BN

KW - Retinal Degeneration/chemically induced

KW - Retinal Ganglion Cells/cytology

U2 - 10.1159/000379753

DO - 10.1159/000379753

M3 - SCORING: Journal article

C2 - 25832811

VL - 53

SP - 162

EP - 167

JO - OPHTHALMIC RES

JF - OPHTHALMIC RES

SN - 0030-3747

IS - 3

ER -