Cited by 50Multiple Sclerosis Research StudiesSphingolipid Metabolism and SignalingFatty Acid Research and Health

Increasing acetyl-CoA metabolism attenuates injury and alters spinal cord lipid content in mice subjected to experimental autoimmune encephalomyelitis

Chevalier, Amber C., Rosenberger, Thad A.·2017·Journal of Neurochemistry

Abstract

Abstract Acetate supplementation increases brain acetyl‐CoA metabolism, alters histone and non‐histone protein acetylation, increases brain energy reserves, and is anti‐inflammatory and neuroprotective in rat models of neuroinflammation and neuroborreliosis. To determine the impact acetate supplementation has on a mouse model of multiple sclerosis, we quantified the effect treatment had on injury progression, spinal cord lipid content, phospholipase levels, and myelin structure in mice subjected to experimental autoimmune encephalomyelitis (EAE). EAE was induced by inoculating mice with a myelin oligodendrocyte glycoprotein peptide fragment (MOG35–55), and acetate supplementation was maintained with 4 g/kg glyceryl triacetate by a daily oral gavage. Acetate supplementation prevented the onset of clinical signs in mice subject to EAE compared to control‐treated mice. Furthermore, acetate supplementation prevented the loss of spinal cord ethanolamine and choline glycerophospholipid and phosphatidylserine in mice subjected to EAE compared to EAE animals treated with water. Treatment increased saturated and monounsaturated fatty acid levels in phosphatidylserine compared to controls suggesting that acetate was utilized to increase spinal cord fatty acid content. Also, acetate supplementation prevented the loss of spinal cord cholesterol in EAE animals but did not change cholesteryl esters. Treatment significantly increased GD3 and GD1a ganglioside levels in EAE mice when compared to EAE mice treated with water. Treatment returned levels of phosphorylated and non‐phosphorylated cytosolic phospholipase A2 (cPLA2) levels back to baseline and based on FluoroMyelin™ histochemistry maintained myelin structural characteristics. Overall, these data suggest that acetate supplementation may modulate lipid metabolism in mice subjected to EAE. image

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Crossref · 10.1111/jnc.14032

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117 of 117 references verified0 citation errors · 0 not checkable

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  • Acetate supplementation induces increased acetyl-CoA metabolism, increases histone acetylation, resulting in preserved spinal cord lipid content and essentially preventing the onset of clinical symptoms of EAE.

    “Specifically, acetate supplementation is able to induce increased acetyl-CoA metabolism, which increases histone acetylation, resulting in preserved spinal cord lipid content and essentially preventing the onset of clinical symptoms of EAE (179).”
  • Short-chain fatty acids favor enhancement of acetyl-CoA metabolism, histone acetylation, preservation of spinal cord lipid content, suppression of demyelination, and oligodendrocyte maturation and differentiation.

    “Mechanistically, SCFAs favor the enhancement of acetyl-CoA metabolism, histone acetylation, preservation of spinal cord lipid content, suppression of demyelination, oligodendrocyte maturation and differentiation (157, 158).”

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Authors
Chevalier, A. C., & Rosenberger, T. A.
Affiliations
University of North Dakota (US)
Corresponding author
Rosenberger, Thad A.
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2017-05-02
Volume
141
Issue
5
Pages
721-737
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W2604611003
Cited by
50
References
117
Citations by year
2025: 4 · 2024: 7 · 2023: 6 · 2022: 21 · 2021: 4 · 2020: 6 · 2019: 1 · 2018: 1
FWCI
1.72
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Funders
UND SMHS Seed Grant
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Multiple Sclerosis Research Studies
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
  • Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
Keywords
acetate supplementation, acetyl-CoA metabolism, experimental autoimmune encephalomyelitis, multiple sclerosis, phospholipase A2, gangliosides, phosphatidylserine, myelin structure, triacetin, neuroinflammation, cholesterol, fatty acid composition, myelin oligodendrocyte glycoprotein
MeSH terms
Acetates, Acetyl Coenzyme A, Animals, Behavior, Animal, Chromatography, Thin Layer, Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental, Fatty Acids, Female, Mice, Inbred C57BL, Myelin Sheath, Peptide Fragments, Spinal Cord, Triglycerides, Statistics, Nonparametric, Lipid Metabolism, Mice, Phospholipases A2, Myelin-Oligodendrocyte Glycoprotein

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