Titlebook: Obesity Before Birth; Maternal and prenata Robert H Lustig Book 2011 Springer Science+Business Media, LLC 2011 GNAS locus.Obesity.Prader-Wi

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The Contribution of Heredity to Clinical Obesitysease. In the last few decades of the twentieth century and into the twenty-first, rates of obesity have greatly increased, initially in the USA, then in other Western industrialized countries until we now have a genuinely global epidemic. As evolution works on a far longer timescale than this, it h

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Genome-Wide Association Studies and Human Population Obesityusceptibility loci for common obesity. GWA studies are hypothesis-generating in that they interrogate hundreds of thousands of genetic variants across the whole human genome for association with a disease or trait of interest without an a priori hypothesis. As such, GWA studies hope to identify new

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Known Clinical Epigenetic Disorders with an Obesity Phenotype: Prader–Willi Syndrome and the , Locushistones by methylation without altering the DNA sequence. Epigenetics is heritable but reversible depending on the parent of origin. PWS is a neurodevelopmental disorder characterized by hypotonia, feeding difficulties, hypogonadism, growth failure, learning/behavioral problems, and hyperphagia in

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Epigenetic Changes Associated with Intrauterine Growth Retardation and Adipogenesisy, and pre- and postnatal exposure to environmental chemicals, also known as obesogens. Epigenetic modifications may be one mechanism by which exposure to an altered intrauterine milieu or metabolic perturbation may influence the phenotype of the organism much later in life. Epigenetic modifications

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Exposure to Diabetes In Utero, Offspring Growth, and Risk for Obesityoming increasingly important to understand how events that happen early in life, even before birth, can alter the obesity trajectory of individuals. The effects of intrauterine exposure to a diabetic pregnancy may permanently alter the offspring’s long-term risk for obesity and metabolic disease. Th

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