Epigenetic mechanisms linking early nutrition to long term health

Centre for Biological Sciences, Institute of Developmental Sciences, Faculty of Natural and Environmental Sciences, University of Southampton, Southampton SO16 6YD, UK. Electronic address: .
Best Practice & Research: Clinical Endocrinology & Metabolism (Impact Factor: 4.6). 10/2012; 26(5):667-76. DOI: 10.1016/j.beem.2012.03.009
Source: PubMed


Traditionally it has been widely accepted that our genes together with adult lifestyle factors determine our risk of developing non-communicable diseases such as type 2 diabetes mellitus, cardiovascular disease and obesity in later life. However, there is now substantial evidence that the pre and early postnatal environment plays a key role in determining our susceptible to such diseases in later life. Moreover the mechanism by which the environment can alter long term disease risk may involve epigenetic processes. Epigenetic processes play a central role in regulating tissue specific gene expression and hence alterations in these processes can induce long-term changes in gene expression and metabolism which persist throughout the lifecourse. This review will focus on how nutritional cues in early life can alter the epigenome, producing different phenotypes and altered disease susceptibilities.

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    • "Although maternal metabolism could not be related to the conformation and glucose metabolism of the newborn calves under field conditions, one has to keep in mind that the metabolic consequences of malnutrition in utero may only emerge around or after puberty. Adaptive metabolic features, in response to a disturbed metabolic environment, can become permanent through altered patterns of gene expression (Lillycrop and Burdge 2012). Epigenetic mechanisms, such as DNA methylation, are crucial in the regulation of gene expression and intense epigenetic modifications occur in germ cells and the preimplantation embryo. "
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    ABSTRACT: Although fragmented and sometimes inconsistent, the proof of a vital link between the importance of the physiological status of the mother and her subsequent reproductive success is building up. High-yielding dairy cows are suffering from a substantial decline in fertility outcome over past decades. For many years, this decrease in reproductive output has correctly been considered multifactorial, with factors including farm management, feed ratios, breed and genetics and, last, but not least, ever-rising milk production. Because the problem is complex and requires a multidisciplinary approach, it is hard to formulate straightforward conclusions leading to improvements on the 'work floor'. However, based on remarkable similarities on the preimplantation reproductive side between cattle and humans, there is a growing tendency to consider the dairy cow's negative energy balance and accompanying fat mobilisation as an interesting model to study the impact of maternal metabolic disorders on human fertility and, more specifically, on oocyte and preimplantation embryo quality. Considering the mutual interest of human and animal scientists studying common reproductive problems, this review has several aims. First, we briefly introduce the 'dairy cow case' by describing the state of the art of research into metabolic imbalances and their possible effects on dairy cow reproduction. Second, we try to define relevant in vitro models that can clarify certain mechanisms by which aberrant metabolite levels may influence embryonic health. We report on recent advances in the assessment of embryo metabolism and meantime critically elaborate on advantages and major limitations of in vitro models used so far. Finally, we discuss hurdles to be overcome to successfully translate the scientific data to the field.
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    • "A more detailed description of epigenetic marks is introduced by Daniel and Tollesfbol in this issue (Daniel and Tollesfbol, 2015). Epigenetics, because of its dynamic nature, can be sensitive to the environment and there is an obvious link between nutrition, energy metabolism and epigenetic processes (Delage and Dashwood, 2008; Choi and Friso, 2010; Gabory et al., 2011; Lillycrop and Burdge, 2012; Kaelin and McKnight, 2013; Vanhees et al., 2014). Briefly, nutrients and their metabolites can be direct substrates of the epigenetic machinery enzymes that appose the epigenetic marks. "
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    ABSTRACT: The recent and rapid worldwide increase in non-communicable diseases challenges the assumption that genetic factors are the primary contributors to such diseases. A new concept of the 'developmental origins of health and disease' (DOHaD) is at stake and therefore requires a paradigm shift. Maternal obesity and malnutrition predispose offspring to develop metabolic syndrome, a vicious cycle leading to transmission to subsequent generation(s), with differences in response and susceptibility according to the sex of the individual. The placenta is a programming agent of adult health and disease. Adaptations of placental phenotype in response to maternal diet and metabolic status alter fetal nutrient supply. This implies important epigenetic changes that are, however, still poorly documented in DOHaD studies, particularly concerning overnutrition. The aim of this review is to discuss the emerging knowledge on the relationships between the effect of maternal nutrition or metabolic status on placental function and the risk of diseases later in life, with a specific focus on epigenetic mechanisms and sexual dimorphism. Explaining the sex-specific causal variables and how males versus females respond and adapt to environmental perturbations should help physicians and patients to anticipate disease susceptibility. © 2015. Published by The Company of Biologists Ltd.
    Full-text · Article · Jan 2015 · Journal of Experimental Biology
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    • "These findings shaped the definition of the term ''epigenetics'' to become the study of modifications in gene expression that do not involve changes in DNA nucleotide sequences [5]. Hence, the epigenetic layer of gene regulation controls both normal cellular processes and abnormal events associated with disease, notably cancer [6] [7]. "
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