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Obesity has been present in the human population at a low frequency for a very long time, most likely caused by rare monogenic or syndromic genetic disease. 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...
The hypothalamus plays a major role in the long-term regulation of body weight in humans. Within the hypothalamus, the leptin–melanocortin system is critical for energy balance, as animal and human studies have shown that disruption of this pathway, which senses peripheral energy stores and signals satiety, leads to the most severe forms of human obesity. The monogenic causes of obesity identified...
Understanding how genetic factors contribute to obesity is key to identifying potential therapeutic avenues of study, but to date the major genetic risk factors that predict an obese phenotype remain elusive. The study of simpler genetic causes of obesity, such as isolated phenotypes or in syndromic form, although of limited relevance to the genetic load of common disease, has nonetheless shown promise...
In the past 3 years, genome-wide association (GWA) studies have revolutionized the field of obesity genetics by establishing at least 15 new genetic-susceptibility 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...
Prader–Willi syndrome (PWS) was the first example in humans of genomic imprinting, an epigenetic phenomenon mediated through modifications of DNA and histones 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,...
There is substantial evidence from epidemiology and from animal models that risk of obesity and its related conditions is modified by the quality of the early life environment, in particular, nutrition, behavior, and exposure to hormones. Such exposures represent signals which act through developmental plasticity to induce variation in the phenotype of the offspring. Induction of alternative phenotypes...
Environmental contributions to the development of childhood obesity may include a suboptimal in utero environment, diabetes and/or obesity in pregnancy, 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...
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