Epigenetic Differences In DNA Methylation

The first major effects of epigenetics on genes can be seen in the role of DNA methylation in mammalian epigenetics. DNA methylation provides a method of gene control in an organism, where it assures proper gene expression, as well as silencing of genes within cells, it does this through the manipulation of chromosome architecture, where it affects the packaging of the DNA by the binding of a methyl group to cytosine (Kullis & Esteller, 2010). The effects of this can

Genetic research of obesity was partly successful in establishing obesity in model organisms – rodents where obesity occurs spontaneously together with other pathological aspects (insulin resistance, …). The main cause of monogenic obesity in these model organisms are common mutations always present in only one gene. Results of research on model organisms allowed us to understand biological mechanisms of calorie intake and regulation and maintenance of body weight. The most important insight into obesity was achieved in 1994 after discovery of ob gene encoding for leptin. In two years period, using screening method, candidate homologous genes, selected on genetic study basis on mice, another five genes were identified. Mutations on these genes were found to be the cause of autosomal recessive or dominant monogenic obesity. Products of these genes are leptin and its receptor, proopiomelanocortin (POMC) melanocortin receptor 4 (MC4R) and

The mapping of human genes has allowed for certain genetic disorders to be identified according to the genes that it is affecting. This has created a map that other individuals' genes can be compared to in order to determine any mistakes or any alterations that may lead to the development of a disease. Any changes in epigenetic

On a molecular level, fat tissue is normally the largest organ in humans and is involved in mechanisms and pathways that deal with longevity. Fat tissue is not only involved in energy storage but is also important in immune and endocrine function, thermoregulation, mechanical protection, and tissue regeneration (Tchkonia et al., 2010). Adipose tissue is able to protect against infection and trauma. It is also able to produce and activate hormones, including IL-6, IGF-1, and glucocorticoids, as well as prevent heat loss (Tchkonia et al., 2010). Throughout life, changes in fat distribution and function is constantly occurring and in older individuals, these changes correspond to a number of health disorders like hypertension, cancers, cognitive dysfunction, and diseases like diabetes, heart attacks, and strokes, as previously noted (Tchkonia et al., 2010). As people age, their body composition increases in fat mass and decreases in muscle mass, regardless of their body weight or BMI (Dorner and Rieder, 2011).

indicate that inherited genetic variation is an important risk factor for obesity. It was also pointed

Prevention is best done early (prior to conception, during pregnancy, or at the latest prior to a child’s third birthday) to optimise the epigenetic ‘set-points’ for the guideline of appetite and fat mass. This would suggest that women who are obese should lose weight before considering pregnancy while, programs during the early years of primary schools are required to optimise healthy weight and prevent chronic disease and disability.

The body can afford to accumulate a little extra fat, but when the fat accumulation exceeds the minimum extent, it interferes with the general health. According to new studies published in the "journal Neurology", researchers has revealed that Americans are not obese because we eat too much, but because it is in our genetic make-up. Researchers believe that genes play a very important role in many cases. People with a history of obesity in one or both parents are at higher risk of becoming obese themselves. Those who have inherited "obesity genes" may use calories at a slower rate than others, or they may not have the same appetite "shutoff" control system that helps lean people stop eating when they have taken in enough

Epigenetics is the study of cellular and physiological traits that are not caused by changes in the DNA sequence but they are triggered by chemical reactions that activate and deactivate parts of the genome and in specific locations. Therefore, epigenetics is the study of chemical reactions and factors that influence them. Hypothetically, epigenetics has the huge potential in terms of the uncovering genetic development of organisms, including humans, and the impact of chemical reactions that occur under the impact of various factors and affect genome activation and deactivation in specific locations. In this regard, further studies and development of epigenetics is essential but the impact and role of epigenetics should not be overestimated

Obesity is a growing problem in America. There are many reasons obesity is growing rapidly such as genetics, physical inactivity, nutrition, medications, diseases, and psychological factors, just to name a few. Something that does not come to mind when speaking about obesity is genetics. But believe it or not, genetics does play a role in obesity just like other causes aforementioned above. Because obesity is a growing problem in America, it is important to understand and act upon its many causes, helping put an end to the sicknesses and deaths derived from it. Many would assume obesity is a result of poor eating habits and lack of exercise, but genetics also play into the issue. This essay will discuss two types of obesity which

“ 1. Adipokines are hormones produced by adipose tissue. /…/ Adipokines have effects not only on tissues but [also] on the hypothalamic and pancreatic function. /…/ 2. Elevated serum free fatty acids and high intracellular deposits of triglycerides and cholesterol. These lead to metabolic overload with interfere of insulin signaling and a decrease in tissue response to insulin. 3. Obesity causes release of inflammatory cytokines. /…/ These play an important role in the genesis of a fatty liver [which impairs the function]. 4.

Researchers first thought the genes you receive from your parents are set in stone since they are made of a genetic code set in our DNA sequence;however, they are discovering that there is a second layer of structure that combines with DNA to decide whether or not a gene is active or not, called the epigenome. The epigenome consists of the DNA, histones, a protein DNA is wrapped around, and chemical tags. The epigenome alters the genetic code by directing signals. The signals come from the environment, which are reacted upon by epigenetic tags to turn a gene either on or off without affecting the DNA sequence. Certain things from our environment that send signals to epigenetic tags to change our genes in the epigenome includes the following:

Sarcopenia is the progressive loss of skeletal muscle mass and function with age. It often is a result of or leads to decrease in physical activity which leads to functional impairement or disability and increases vulnerability towards other chronic ailments such as cardiovascular disease, insulin resistance, type 2 diabetes etc (Roubenoff & Hughes 2000). With age there is a decline in mitochondrial biogenesis as well as reduction in the ability to promote muscle protein synthesis which has substantial impact on the age-associated loss of muscle mass and strength, both of which are the two most recognized risk phenotypes associated with sarcopenia. Previous work has reported enormous inter-individual variability in these phenotypes arising

Moving from a genetic predisposition to obesity itself usually requires an adjustment in an individual’s eating habits, regime, or other environmental factors. Having a better grasp of what contributes to the genetics of obesity, especially common obesity-and gene-environment relations, will produce a better understanding of the pathways that lead to obesity. Such data could someday produce favorable tactics for obesity treatment and prevention. But it’s imperative to remember that generally, the impact of genes to obesity possibility is minor, while the influence of our activity environment and toxic food is enormous. As one scientist wrote, “Genes may co-determine who becomes obese, but our environment determines how many become obese.” (20) Which is why obesity prevention efforts must be at the forefront on changing our environment to make healthier choices and stress-free choices, for

Human development from conception to adulthood is a conjoined partnership, moulded within our cells, of Nature (the DNA we inherit) and Nurture (the prevailing nutritional, social and physical environment). The field of epigenetic is quickly growing and with it the understanding that both the environment and individual lifestyle can also directly interact with the genome to influence epigenetic change. Developing organisms seem to have a wide range of susceptibility to epigenetic changes. Appropriate dynamics in epigenetic modifications are essential for embryogenesis, early fetal development and early postnatal growth. Consequently, the inadequate establishment of epigenetic modifications during critical developmental periods due to changes

The condition of obesity occurs when an individuals has accrued bodily fat to the point where it has a detrimental influence on their well-being. In the event that an individual’s bodily fat is 20% more elevated than normal, the person would be considered as being obese. In the event that the bodily mass index, (BMI) is found in the range of 25 to 29.9, the person would be considered as overweight. In the circumstance that the bodily mass index is more than 30, the person would be considered as obese. People become obese due to the intake of too many calories. In the year 2000, it had been assessed that over 30% of the United States’ population was considered as obese. In addition, individuals who have a sedentary lifestyle are at risk of obesity. The less movement that an individual engages, the less potential of burning calories. In addition, insufficient sleep has increased the risk of obesity. Furthermore, there are some hormone disruptors which cause the metabolising of fructose in the liver. Finally, there are many who are obese due to their genetic predisposition. There is a defective gene that is delineated ass FTO. This gene is the cause of 16.6% of people having the quality of being obese (Medical News Today 2015).