Leptin receptor gene q223r polymorphism in young urban Sri Lankan women
Introduction
Overweight and obesity result from fat accumulation in adipose tissue which is an important fact occur in result of energy imbalance and associated with many chronic diseases. The risk of becoming overweight/obese with this fat accumulation increases across all socio-economic classes as a result of urbanization, which expose them to an obesogenic environment. A relatively high prevalence of overweight and obesity has been identified in Sri Lankan urban population, especially females (Katulanda, et al., 2010). Genetics plays an important role in obesity (Loos et al, 2009). Twin studies states also supports the fact that genetic influences are notable in obesity (Bouchard, et al,1990). Genetic composition can predispose an individual to weight gain in this obesogenic environment which arises with urbanization.
Different SNPs in the lep R have been associated with overwitght / obesity. SNP- Q223R in extracellular domain of leptin receptor gene, results in the nucleotide substitution, Adenine to Guanine due to condon change occurs at 223rd position which is a non-conservative amino acid change. This amino acid change placed in first cytokine receptor homology, in between two FNIII-like sub-domains and can affect the function of Lep Rs in hypothalamus and placenta as well as soluble leptin receptors in energy homiostasis.
Although BMI has been widely used for accesses obesity, it does not
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
Genes control almost every aspect of human life, and when it comes to weight there is no exception. Little is known, however, how much of an individual’s genes actually control the weight of certain individuals. Body fat can vary from person to person, yet some people have always carried more weight than others. Often times, when one person is overweight in the family, most of the other individuals in the same family are overweight as well. However, more than just genetics can go into being overweight, and a person’s genes are not the end all be all of obesity. Many times the environment surrounding people who are obese contributes to the overall weight of the individual, and when obesity promoting genes are mixed
The nutrition transition and the increasing westernization, urbanization and mechanization occurring in most countries around the world is associated with changes in the diet towards one of high fat, high energy-dense foods and a sedentary lifestyle (Popkin, 2001). This shift is also associated with the current rapid changes in childhood and adult obesity. Even in many low income countries, obesity is now rapidly increasing, and often coexists in the same population with chronic under nutrition.
Adult obesity rates have rapidly increased since 1960, with at least one-third of the population classified as obese today. It is believed that 60-70% of the risk factors for developing obesity are genetic and are genes that are generally considered to dictate food intake. The environment also significantly affects an individual’s risk for obesity, and poverty level is a huge factor as well. Of the ten states with the highest obesity rates, nine of them among the nation’s poorest states.
indicate that inherited genetic variation is an important risk factor for obesity. It was also pointed
Obesity is a growing problem worldwide. Obesity causes serious health problems and is associated with substantial economic burdens in today's society. In the past, several generic epidmiological approaches have been use to identify genetic linkage to obesity. Evidence has developed that suggest obesity involved hormones and neurotransmitters hypothesized. Obesity is thought to be environmental since, food is plentiful year around.
A few cross-sectional studies examine the association between CRP and obesity, and they found a significant relationship. A systematic review study investigates the association between the CRP and obesity by using body mass index measure
The topic that I have chosen to look at is obesity. The aim of this topic is to find out whether “the ignorance of genetics as a contra factor of obesity”. I have chosen to look at this topic because obesity is concerns me. Obesity has always been a bid debate for a long time now and I was intrigued to find out more about the topic and the cause of obesity. The fact that obesity has made deadlines news in recent years. There are a lot of misconceptions about obesity such as overweight is caused by a sow metabolism. There have been a lot of beliefs and myths about obesity in society today and he above myths is on of them. According to Donnellan (1998) ‘ ‘people who are overweight have told their doctors that they eat no more and
Obesity has become an epidemic health problem. It is not only about genetics but also the environmental factors involved in obesity. According to Kaushik Prashant and James T. Anderson Epigenetic it is the study of heritable but the dynamic changes to genomic function that regulate gene expression independently of DNA sequence. The study have shown that the maternal nutrition is controlled during pregnancy that can alter the metabolic phenotype of the offspring by means of epigenetic regulation of specific genes, and this can be passed to the next generation. Obesity is associated with extensive gene expression changes throughout the body. It is a simple disease with multiple risk factors.
For the Asian Indian population, disease prevention or management interventions should be designed keeping in mind their unique body composition and predisposition to chronic conditions such as insulin resistance, CHD and metabolic syndrome. Given the predilection for excess abdominal adiposity at a normal BMI predisposing the
It affects the hypothalamus through negative feedback, to control appetite and energy expenditure, with elevated blood levels in obese individuals.
Leptin is a hormone that is produced by the body’s fat cells. It is called the “satiety hormone”. The target cells of Leptin are found in the hypothalamus. The main function of leptin is to tell the brain that there is enough fat in our body so that we lose appetite. When the amount of fat decreases, the level of plasma leptin falls so that appetite is stimulated until the fat mass is recovered. And when fat mass increases, so do leptin levels and appetite is suppressed until weight loss occurs. Leptin levels fell during weight loss and increased brain activity in areas involved in emotional, cognitive, and sensory control of food intake. Restoration of leptin levels maintained weight loss and reversed the changes in brain activity. Thus, leptin is a critical factor linking reduced energy stores to eating behavior. Potentially, leptin therapy could sustain weight loss by overriding the tendency toward energy conservation. Obesity increases the risk of diabetes, coronary artery disease, fatty liver, gallstones, sleep apnea, arthritis, and cancer and may shorten the
During the research, it is found that triacylglycerols and fatty acids are not the only reason for people to become obese. Genetic factors are also a part of reasons for obesity. The gene decides some people are born with a tendency to obesity and this theory is based on the ‘Thrifty gene hypothesis’ raised by geneticist James V. Neel in 1962. The idea of ‘Thrifty gene hypothesis’ is that in ancient times, for hunter-gather populations ‘Thrifty gene’ would allow them to fatten more quickly when they have enough food. This is an advantage for them because with ‘Thrifty gene’ they can survive the famine. But in modern societies, this gene is useless because people have sufficient food and they don’t need to worry about
Cytokine signaling-3 is an intracellular protein that suppresses the actions of many different cytokine receptors. It can limit leptin signaling and is potentially one of the causes of leptin resistance (Coll et al. 2007). In a study conducted, it was observed that obese subjects who lost weight had decreased concentrations of leptin that would rise slightly once their lowered weight was maintained, suggesting that leptin tracks body fat during weight gain as well as weight loss (Campfield et al. 1996). This also suggests that in the presence of extended exposure to low leptin concentrations, the leptin pathway can be reset and allow for more sensitivity to leptin (Campfield et al.
Fat kids are always considered cute, parents and elderly people have the myth that it’s a healthy sign and represents the family’s wealth. Parents and elders in the family pamper kids and feed them all the high calorie foods and make them obese at a very young age. Child obesity is increasing terribly in India. It is hard to believe as in the same country you find thousands of homeless children who are deprived of food, nutrition and essential facilities. Many factors are linked with child obesity in India, especially it is identified that kids who belong to the upper middle class and wealthy family fall prey to obesity. Heredity, biological factors, eating habits, etc. are all some of the causes for child obesity. In common, when you don’t spend the energy that comes from food and fail to indulge in physical activity, you accumulate more fat.