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Abstract
Studies in human and animals have demonstrated that nutritionally induced low birth-weight followed by rapid postnatal growth increases the risk of metabolic syndrome and cardiovascular disease. Although the mechanisms underlying such nutritional programming are not clearly defined, increased oxidative-stress leading to accelerated cellular aging has been proposed to play an important role. Using an established rodent model of low birth-weight and catch-up growth, we show here that post-weaning dietary supplementation with coenzyme Q10, a key component of the electron transport chain and a potent antioxidant rescued many of the detrimental effects of nutritional programming on cardiac aging. This included a reduction in nitrosative and oxidative-stress, telomere shortening, DNA damage, cellular senescence and apoptosis. These findings demonstrate the potential for postnatal antioxidant intervention to reverse deleterious phenotypes of developmental programming and therefore provide insight into a potential translatable therapy to prevent cardiovascular disease in at risk humans.
Highlights
It has been known for several years that low birth weight babies have significantly increased risk of developing the metabolic syndrome and cardiovascular disease (CVD) in later life [1,2,3,4]
By day 14, this group had undergone accelerated postnatal growth the body weights were similar between groups [32.57 1.3 g vs 32.0 7 1.3 g]
P47phox protein expression was significantly higher in the recuperated group compared to controls, but this was not prevented by CoQ10 supplementation
Summary
It has been known for several years that low birth weight babies have significantly increased risk of developing the metabolic syndrome and cardiovascular disease (CVD) in later life [1,2,3,4]. These findings led to the proposal of the ‘Thrifty Phenotype Hypothesis’ [5], which postulates that under conditions of sub-optimal in-utero nutrition, the fetus permanently alters its organ structure and function to ensure immediate survival of the organism. Reactive oxidative species (ROS) and reactive nitrogen species (RNS) are collectively known as reactive inflammatory species (RIS) [21] These can accumulate during cardiovascular aging [22,23] and can cause damage to DNA, protein and lipids. Short telomeres are known to activate a series of DNA damage checkpoint proteins including p53, p21 and p16INK, which can induce
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