Abstract:
:We have previously shown that induction of ketosis by ketogenic diet (KD) conveyed neuroprotection following spinal cord injury in rodent models, however, clinical translation may be limited by the slow raise of ketone levels when applying KD in the acute post-injury period. Thus we investigated the use of exogenous ketone supplementation (ketone sodium, KS) combined with ketogenic diet as a means rapidly inducing a metabolic state of ketosis following spinal cord injury in adult rats. In uninjured rats, ketone levels increased more rapidly than those in rats with KD alone and peaked at higher levels than we previously demonstrated for the KD in models of spinal cord injury. However, ketone levels in KD + KS treated rats with SCI did not exceed the previously observed levels in rats treated with KD alone. We still demonstrated neuroprotective effects of KD + KS treatment that extend our previous neuroprotective observations with KD only. The results showed increased neuronal and axonal sparing in the dorsal corticospinal tract. Also, better performance of forelimb motor abilities were observed on the Montoya staircase (for testing food pellets reaching) at 4 and 6 weeks post-injury and rearing in a cylinder (for testing forelimb usage) at 6 and 8 weeks post-injury. Taken together, the findings of this study add to the growing body of work demonstrating the potential benefits of inducing ketosis following neurotrauma. Ketone salt combined with a ketogenic diet gavage in rats with acute spinal cord injury can rapidly increase ketone body levels in the blood and promote motor function recovery. This study was approved by the Animal Care Committee of the University of British Columbia (protocol No. A14-350) on August 31, 2015.
journal_name
Neural Regen Resjournal_title
Neural regeneration researchauthors
Tan BT,Jiang H,Moulson AJ,Wu XL,Wang WC,Liu J,Plunet WT,Tetzlaff Wdoi
10.4103/1673-5374.280327subject
Has Abstractpub_date
2020-10-01 00:00:00pages
1912-1919issue
10eissn
1673-5374issn
1876-7958pii
NeuralRegenRes_2020_15_10_1912_280327journal_volume
15pub_type
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journal_title:Neural regeneration research
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journal_title:Neural regeneration research
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doi:10.4103/1673-5374.153690
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journal_title:Neural regeneration research
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doi:10.4103/1673-5374.141791
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journal_title:Neural regeneration research
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journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.4103/1673-5374.295347
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journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.3969/j.issn.1673-5374.2012.18.003
更新日期:2012-06-25 00:00:00
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journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.3969/j.issn.1673-5374.2012.21.002
更新日期:2012-07-25 00:00:00
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journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.3969/j.issn.1673-5374.2012.14.008
更新日期:2012-05-15 00:00:00
abstract::Amyloid β peptide binding alcohol dehydrogenase (ABAD) decoy peptide (DP) can competitively antagonize binding of amyloid β peptide to ABAD and inhibit the cytotoxic effects of amyloid β peptide. Based on peptide aptamers, the present study inserted ABAD-DP into the disulfide bond of human thioredoxin (TRX) using mole...
journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.3969/j.issn.1673-5374.2013.01.005
更新日期:2013-01-05 00:00:00
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pub_type: 杂志文章,评审
doi:10.4103/1673-5374.243701
更新日期:2019-01-01 00:00:00
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journal_title:Neural regeneration research
pub_type: 杂志文章
doi:10.4103/1673-5374.259624
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journal_title:Neural regeneration research
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doi:10.4103/1673-5374.158368
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journal_title:Neural regeneration research
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doi:10.3969/j.issn.1673-5374.2012.34.001
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journal_title:Neural regeneration research
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abstract::[This corrects the article DOI: 10.4103/1673-5374.245480]. ...
journal_title:Neural regeneration research
pub_type: 杂志文章,已发布勘误
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