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Supplementation with the reduced form of Coenzyme Q 10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator‐activated receptor‐α gene expression signature in SAMP1 mice
Author(s) -
Schmelzer Constance,
Kubo Hiroshi,
Mori Masayuki,
Sawashita Jinko,
Kitano Mitsuaki,
Hosoe Kazunori,
Boomgaarden Inka,
Döring Frank,
Higuchi Keiichi
Publication year - 2010
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.200900155
Subject(s) - peroxisome proliferator activated receptor , coenzyme q – cytochrome c reductase , biology , endocrinology , senescence , kidney , receptor , medicine , gene expression , inflammation , phenotype , gene , biochemistry , microbiology and biotechnology , immunology , cytochrome c , mitochondrion
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.