Nutritional programming of coenzyme Q: potential for prevention and intervention?

Low birth weight and rapid postnatal growth increases risk of cardiovascular‐disease (CVD); however, underlying mechanisms are poorly understood. Previously, we demonstrated that rats exposed to a low‐protein diet in utero that underwent postnatal catch‐up growth (recuperated) have a programmed defi...

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Bibliographic Details
Published in:The FASEB journal 2014-12, Vol.28 (12), p.5398-5405
Main Authors: Tarry‐Adkins, Jane L., Fernandez‐Twinn, Denise S., Chen, Jian‐Hua, Hargreaves, Iain P., Martin‐Gronert, Malgorzata S., McConnell, Josie M., Ozanne, Susan E.
Format: Article
Language:English
Subjects:
aging
Animals
cardiovascular disease
Cardiovascular Diseases - enzymology
Cardiovascular Diseases - prevention & control
Dietary Supplements
Female
Oxidative Stress
Pregnancy
Rats, Wistar
Research Communications
Telomerase - metabolism
telomeres
Ubiquinone - administration & dosage
Ubiquinone - metabolism
vascular disease
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Summary:Low birth weight and rapid postnatal growth increases risk of cardiovascular‐disease (CVD); however, underlying mechanisms are poorly understood. Previously, we demonstrated that rats exposed to a low‐protein diet in utero that underwent postnatal catch‐up growth (recuperated) have a programmed deficit in cardiac coenzyme Q (CoQ) that was associated with accelerated cardiac aging. It is unknown whether this deficit occurs in all tissues, including those that are clinically accessible. We investigated whether aortic and white blood cell (WBC) CoQ is programmed by suboptimal early nutrition and whether postweaning dietary supplementation with CoQ could prevent programmed accelerated aging. Recuperated male rats had reduced aortic CoQ [22 d (35±8.4%; P
ISSN:0892-6638
1530-6860
DOI:10.1096/fj.14-259473