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Review article| Volume 266, P31-40, November 2017

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Epigenetic programming, early life nutrition and the risk of metabolic disease

  • Tomasz Block
    Affiliations
    Epigenetics in Human Health and Disease Laboratory, Central Clinical School, Faculty of Medicine, Monash University, Victoria 3004, Australia
    Search for articles by this author
  • Assam El-Osta
    Correspondence
    Corresponding author. Epigenetics in Human Health and Disease Laboratory, Central Clinical School, Faculty of Medicine, Monash University, Victoria 3004, Australia.
    Affiliations
    Epigenetics in Human Health and Disease Laboratory, Central Clinical School, Faculty of Medicine, Monash University, Victoria 3004, Australia

    Department of Pathology, The University of Melbourne, Parkville, Victoria, Australia

    Hong Kong Institute of Diabetes and Obesity, Prince of Wales Hospital, The Chinese University of Hong Kong, Hong Kong Special Administrative Region
    Search for articles by this author

      Highlights

      • Adult health and disease are traced to fetal origins and early life factors.
      • Parental diet regulates epigenetic modification and the risk of metabolic disease in offspring.
      • Nutrient sensing of metabolic status and homeostasis is controlled centrally by the hypothalamus.
      • Hypothalamus interpret extracellular cues to control energy balance by regulating epigenetic information and gene expression.

      Abstract

      Time separates the past from the present, during this period memory are formed - written in code and decoded to be read while other memories are erased - but when it comes to the epigenome some memories are harder to forget than others. Recent studies show chemical information is written in the context of the epigenome and codified on histone and non-histone proteins to regulate nuclear processes such as gene transcription. The genome is also subject to modification in the form of 5-methylcytosine, which has been implicated in metabolic memory. In this review, we examine some of the chemical modifications that signal early life events and explore epigenetic changes that underlie the diabetic vasculature. The fine balance between past and present is discussed, as it pertains to gestational diabetes and obesity in context to the Barker hypothesis. We also examine emerging experimental evidence suggesting the hypothalamus as a central regulator of obesity risk and explore current genomic medicine. As for how cells recall specific chemical information, we examine the experimental evidence implicating chemical cues on the epigenome, providing examples of diet during pregnancy and the increased risk of disease in offspring.

      Graphical abstract

      Keywords

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