Cited by 53Coenzyme Q10 studies and effectsGenetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and Senescence

Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator‐activated receptor‐α gene expression signature in SAMP1 mice

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Schmelzer, Constance, Kubo, Hiroshi, Mori, Masayuki, Sawashita, Jinko, Kitano, Mitsuaki, Hosoe, Kazunori, Boomgaarden, Inka, Döring, Frank +1 more·2010·Molecular Nutrition & Food Research

Abstract

Our present study reveals significant decelerating effects on senescence processes in middle‐aged SAMP1 mice supplemented for 6 or 14 months with the reduced form (Q 10 H 2, 500 mg/kg BW/day) of coenzyme Q 10 (CoQ 10). To unravel molecular mechanisms of these CoQ 10 effects, a genome‐wide transcript profiling in liver, heart, brain and kidney of SAMP1 mice supplemented with the reduced (Q 10 H 2) or oxidized form of CoQ 10 (Q 10) was performed. Liver seems to be the main target tissue of CoQ 10 intervention, followed by kidney, heart and brain. Stringent evaluation of the resulting data revealed that Q 10 H 2 has a stronger impact on gene expression than Q 10, primarily due to differences in the bioavailability. Indeed, Q 10 H 2 supplementation was more effective than Q 10 to increase levels of CoQ 10 in the liver of SAMP1 mice. To identify functional and regulatory connections of the “top 50” (p<0.05) Q 10 H 2‐sensitive transcripts in liver, text mining analysis was used. Hereby, we identified Q 10 H 2‐sensitive genes which are regulated by peroxisome proliferator‐activated receptor‐α and are primarily involved in cholesterol synthesis (e.g. HMGCS1, HMGCL and HMGCR), fat assimilation (FABP5), lipoprotein metabolism (PLTP) and inflammation (STAT‐1). These data may explain, at least in part, the decelerating effects on degenerative processes observed in Q 10 H 2‐supplemented SAMP1 mice.

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  • The outperformance of CoQ10H2 could be at least in part explained by a higher CoQ10H2 bioavailability at the same concentrations, allowing a more efficient subcellular delivery.

    “The reason for this outperformance could be at least in part explained by a higher CoQ10H2 bioavailability at the same concentrations, therefore allowing a more efficient subcellular delivery [66,71].”
  • CoQ10H2 (ubiquinol) is even more efficient than CoQ10 itself in reverting senescence markers expression, both in vitro and in vivo.

    “CoQ10H2 (or ubiquinol), the reduced form of CoQ10, is even more efficient than CoQ10 itself in reverting senescence markers expression, both in vitro and in vivo [66,71].”

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Authors
Schmelzer, C., Kubo, H., Mori, M., Sawashita, J., Kitano, M., Hosoe, K., Boomgaarden, I., Döring, F., & Higuchi, K.
Affiliations
  • Christian-Albrechts-Universität zu Kiel (DE)
  • Kaneka (Japan) (JP)
  • Shinshu University (JP)
Corresponding author
Döring, Frank
Venue
Molecular Nutrition & Food Research
Publisher
Wiley
Published
2010-06
Volume
54
Issue
6
Pages
805-815
ISSN
  • 1613-4125 (ISSN-L)
  • 1613-4133
OpenAlex
W1995774391
Cited by
53
References
56
Citations by year
2026: 2 · 2025: 1 · 2024: 2 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 5 · 2019: 7 · 2018: 2 · 2017: 3 · 2016: 1 · 2015: 6 · 2014: 5 · 2013: 3 · 2012: 2
FWCI
1.21
Type
journal article
Language
en
Open access
Locations
  • Molecular Nutrition & Food Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
Japan Society for the Promotion of Science (21650097)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Coenzyme Q10 studies and effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Keywords
coenzyme Q10, aging, senescence, SAMP1 mice, PPARα, gene expression signatures, liver, cholesterol biosynthesis, lipoprotein metabolism, inflammation, bioavailability, dietary supplementation
MeSH terms
Aging, Animals, Eating, Female, Gene Expression Regulation, Liver, Oxidation-Reduction, Phenotype, Ubiquinone, Dietary Supplements, Gene Expression Profiling, PPAR alpha, Mice

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