Guide OBESITY GENES and their Epigenetic Modifiers

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Epigenetics and Human Disease

Good enough People. A creatively compelling approach to the possibility that we can press a restart button with A creatively compelling approach to the possibility that we can press a restart button with regard to toxic assumptions we've been raised to believe about human spirituality. Using the artistic ceramic process as metaphor for our lifelong human journey, and CreateSpace Publishing. Genetic changes in human populations occur too slowly to be responsible for the obesity epidemic. Nevertheless, the variation in how people respond to the same environment suggests that genes do play a role in the development of obesity.

Genes give the body instructions for responding to changes in its environment. Studies of resemblances and differences among family members, twins, and adoptees offer indirect scientific evidence that a sizable portion of the variation in weight among adults is due to genetic factors.

Other studies have compared obese and non-obese people for variation in genes that could influence behaviors such as a drive to overeat, or a tendency to be sedentary or metabolism such as a diminished capacity to use dietary fats as fuel, or an increased tendency to store body fat. These studies have identified variants in several genes that may contribute to obesity by increasing hunger and food intake.

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Rarely, a clear pattern of inherited obesity within a family is caused by a specific variant of a single gene monogenic obesity. Most obesity, however, probably results from complex interactions among multiple genes and environmental factors that remain poorly understood multifactorial obesity.

Any explanation of the obesity epidemic has to consider both genetics and the environment. Other hypotheses have been proposed including a role for the gut microbiome as well as early life exposures associated with epigenetic changes. Robust demonstration of the phenomenon in animal models, although, is lacking. Moreover, limitations in access to human tissues from fetal and corresponding adult sources have hampered human research.

This topic is likely to continue to be debated in science and public health policy until more data can be generated to substantiate the hypothesis or not. The effect of the exposure of pregnant women to famine is a related topic. It is well documented that poor nutrition increases the risk of NTDs and folic acid supplementation can reduce the incidence of NTDs. The best example of how early experiences and maternal behavior might alter the mammalian epigenotype has so far been described only in rats. Frequent licking and grooming by rat mothers altered the DNA methylation status in the promoter region of the glucocorticoid receptor GR gene in the hippocampus of their pups.

The highly licked and groomed pups have decreased DNA methylation and increased histone acetylation at the GR promoter compared with pups that were raised by low-licking and -grooming mothers Weaver et al. The increased levels of GR, secondary to the epigenotype change, affect the regulation of stress hormone levels and lifelong response to stress in the rat pups Liu et al. This and follow-up studies in humans answer and raise new questions, driving research toward an understanding of the role of early experiences in modulating epigenotypes and risk for psychiatric disorders.

During the next decade, we anticipate that mutations that alter the epigenotype will become increasingly recognized as mutational mechanisms that cause a variety of human disorders. Traditionally, the identification of disease-causing genes has focused on disorders in which familial cases or patients with chromosomal abnormalities facilitated the positional cloning of the responsible gene.

At this time, we are challenged as we attempt to discover the mutational bases for some of the most common and devastating disorders, such as schizophrenia, autism, and mood disorders. Familial cases are not very common, genetic heterogeneity is very likely, and, last but not least, genetic data—especially the rate of discordances in monozygotic twins—do not always support a straightforward Mendelian inheritance model.

These findings, coupled with the strong environmental effects on the penetrance of some of these disorders, underscore the importance of investigating the epigenomes in such diseases. Even single-gene disorders, such as AS, BWS, and SRS, can be caused either by genomic mutations or mutations that affect the epigenotype, and either inherited or de novo. Such molecular variations will undoubtedly be unearthed for other human disorders. Furthermore, data demonstrating that the levels of several proteins involved in epigenetic regulation are tightly regulated and perturbations of such levels, either through loss-of-function mutations or duplications, cause human disorders suggest that epigenetic mutations that will affect transcription, RNA splicing, or protein modifications are also likely to cause disease.

We thank Dr. Bestor, Dr. Robert A. Rollins, and Dr. Driscoll for the image of a PWS patient, Dr. Bacino for the image of an AS patient, Dr. Glaze for the image of an RTT patient, Dr. Warren for the image of an FXS patient, and Dr. Igna Van den Veyver for input on recurrent hydatidiform moles. We regret that because of space constraints, we had to eliminate many important and relevant citations. Editors: C. Additional Perspectives on Epigenetics available at www. Epigenetics and Human Disease Huda Y.

Zoghbi 1 , 2 and Arthur L. Previous Section Next Section. Figure 1. Figure 2. Figure 3. View this table: In this window In a new window. Table 1. Selected disorders of genomic imprinting. Figure 4. Figure 5. Table 2. Figure 6. Table 3. Figure 7. Figure 8. Figure 9. Previous Section.

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