MedicalResearch.com Interview with: Jane Tarry-Adkins BSc Biochemistry Research Assistant University of Cambridge · Institute of Metabolic Science

Medical Research: What is the background for this study? What are the main findings? Response: From epidemiological and animal studies, it has been known for several years that a suboptimal in utero environment that causes low birth weight combined with accelerated postnatal growth is strongly linked to increased risk of cardiovascular disease (CVD). However underlying molecular mechanisms for this phenomenon, known as ‘developmental programming’ are still unknown. In this study, we used a rat model where animals are born small because their mother ate a low protein diet during pregnancy but grow quickly during lactation when they are suckled by a control diet fed mum. These ‘recuperated’ rats displayed indices of accelerated aortic cellular aging and damage which was associated with a deficit in coenzyme Q (CoQ); (the most abundant endogenous antioxidant in the body), compared to offspring of a normal birth-weight. When these ‘recuperated’ offspring were supplemented with a clinically relevant dose of coenzyme Q, this corrected these markers of aortic cellular aging and aortic damage. Importantly, measurement of CoQ in white blood cells (WBCs) a clinically accessible tissue demonstrated a coenzyme Q deficit in these ‘recuperated’ offspring. Importantly, this strongly correlated with aortic CoQ levels. Furthermore, we also showed a highly significant relationship between CoQ levels and aortic telomere length in WBCs, suggesting that low WBC CoQ levels can predict short aortic telomeres, and therefore susceptibility to aortic disease. (more…)