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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
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Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

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

Jane L Tarry-Adkins1, Denise S Fernandez-Twinn2, Jian-Hua Chen2

  • 1Metabolic Research Laboratories, Institute of Metabolic Science, University of Cambridge, Cambridge, UK; and janeadkins@googlemail.com.

FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology
|August 31, 2014
PubMed

Insights

Early life nutrition impacts cardiovascular health. Supplementing with coenzyme Q (CoQ) in at-risk individuals may prevent programmed aging and reduce cardiovascular disease risk.

Area of Science:

  • Biomedical Science
  • Nutritional Science
  • Cardiovascular Research

Background:

  • Low birth weight and rapid postnatal growth are linked to increased cardiovascular disease (CVD) risk.
  • Underlying mechanisms remain unclear, but programmed deficits in cardiac coenzyme Q (CoQ) and accelerated aging were previously observed in rats.
  • It is unknown if this CoQ deficit extends to clinically accessible tissues.

Purpose of the Study:

  • To investigate if suboptimal early nutrition programs CoQ deficits in the aorta and white blood cells (WBCs) in rats.
  • To determine if postweaning dietary CoQ supplementation can prevent programmed accelerated aging.
  • To explore the potential of WBC CoQ levels as a diagnostic marker for vascular aging.

Main Methods:

  • Rats were exposed to a low-protein diet in utero and underwent postnatal catch-up growth (recuperated).
  • Aortic and WBC CoQ levels, aortic telomere length, DNA damage, oxidative stress markers, and mitochondrial activity were assessed.
  • Some recuperated rats received postweaning dietary CoQ supplementation.

Main Results:

  • Recuperated rats showed significantly reduced aortic CoQ levels at both 22 days and 12 months.
  • Accelerated aortic telomere shortening, increased DNA damage, oxidative stress, and decreased mitochondrial complex II-III activity were observed in recuperated rats.
  • Postweaning CoQ supplementation prevented these detrimental programming effects.
  • Recuperated WBCs also exhibited reduced CoQ, and WBC CoQ levels strongly correlated with aortic telomere length.

Conclusions:

  • Suboptimal early nutrition programs CoQ deficits in the aorta and WBCs, contributing to accelerated vascular aging.
  • Early intervention with CoQ supplementation can prevent these programmed effects.
  • WBC CoQ levels may serve as a valuable, non-invasive diagnostic marker for vascular aging in at-risk individuals.
  • CoQ supplementation represents a potential cost-effective strategy to mitigate the global burden of CVDs.

Keywords:
agingcardiovascular diseasetelomeresvascular disease

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