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Triple-Knockout, Synuclein-Free Mice Display Compromised Lipid Pattern.

Irina A Guschina1, Natalia Ninkina1,2, Andrei Roman1,2

  • 1School of Biosciences, Cardiff University, Cardiff CF10 3AX, UK.

Molecules (Basel, Switzerland)
|June 2, 2021
PubMed
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Synuclein deficiency significantly alters lipid metabolism, affecting fatty acid synthesis, liver lipid storage, and reducing essential brain lipids like plasmalogens. These changes are more pronounced than previously observed with single synuclein deficiencies.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Metabolomics

Background:

  • Synucleins are implicated in lipid biosynthesis and membrane functions.
  • Their role in lipid metabolism, particularly in Parkinson's disease pathogenesis, is under-recognized.
  • Understanding synuclein's broader functions requires studying the combined effects of its family members.

Purpose of the Study:

  • To investigate the impact of complete synuclein deficiency on fatty acid and lipid profiles.
  • To analyze changes in plasma, liver, and brain tissues of triple synuclein-knockout (TKO) mice.
  • To elucidate the role of synucleins in lipid metabolism and potential links to neurological disorders.

Main Methods:

  • Analysis of fatty acids and lipids in plasma, liver, and brain regions of TKO mice.
Keywords:
fatty acidsnon-polar lipidsphospholipidssynucleinstriple-knockout mouse model

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  • Quantification of long-chain polyunsaturated fatty acids (LCPUFA), palmitic acid, triacylglycerol (TAG), and non-esterified fatty acids.
  • Assessment of lipid classes including phosphatidylcholine (PC), cerebrosides (CER), and ethanolamine plasmalogens.

    • Main Results:

    • Synuclein deficiency altered LCPUFA and palmitic acid levels in liver and plasma.
    • Reduced triacylglycerol accumulation in the liver and non-esterified fatty acids in plasma were observed.
    • Significant reduction in ethanolamine plasmalogens and counterbalanced changes in PC and CER were noted in the midbrain.

    Conclusions:

    • Complete synuclein deficiency profoundly impacts PUFA synthesis, hepatic lipid storage, and specific lipid classes.
    • The reduction in plasmalogens and cerebrosides in TKO mice suggests a link to neurological dysfunction.
    • Ablation of all three synucleins leads to more extensive lipid metabolism alterations than previously reported for single synuclein deficiencies.