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The role of FTO gene polymorphism in weight loss: An evidence-based case report
Published in Ade Gafar Abdullah, Isma Widiaty, Cep Ubad Abdullah, Medical Technology and Environmental Health, 2020
The patient stated that his friend advised him to carry out a genetic examination of the FTO gene, and asked if the test was necessary. Based on this clinical scenario, a question arose whether the FTO gene plays a role in the effectiveness of lifestyle modification in obese patients.
Genetics, Epigenetics, and Microbiome
Published in Emily Crews Splane, Neil E. Rowland, Anaya Mitra, Psychology of Eating, 2019
Emily Crews Splane, Neil E. Rowland, Anaya Mitra
Epigenetics refers to changes, sometimes heritable, in gene expression or phenotype caused by mechanisms other than alterations in the nucleotide sequence of DNA. Such changes would not show up in the genetic screens discussed so far. The two well-established epigenetic mechanisms are methylation and histone modification (Figure 4.2). Methylation occurs when a methyl group is added to specific DNA base (s) and interferes with the transcription of the gene. One of the apparent functions of the FTO gene (which encodes the fat mass and obesity associated protein), is to remove methyl groups from certain gene(s) and so influence the normal balance or ratio of translated proteins in the cell. Another epigenetic mechanism is the potential action of the vast non-coding regions of DNA on transcription of coding regions. One important difference between genetics and epigenetics is the time frame: Epigenetics plays out within the lifetime of an individual (and also may be heritable) and is much more consistent with the time-frame for the population-wide rapid increase in BMI.
What Are Eating Disorders?
Published in Jonna Fries, Veronica Sullivan, Eating Disorders in Special Populations, 2017
Epigenetics might offer a bridge to some of the gaps in knowledge about how specific risk factors translate into increased risk for eating disorder development, and they may also offer a way to explain the common theory that parental behaviors are a causative agent in eating disorder development. For example, stress during pregnancy may increase fetal glucocorticoid exposure, which could have adverse health consequences including alterations in function of the HPA axis. Candidate genes for study in terms of epigenetics and risk for eating disorders include the fat mass and obesity-related (FTO) gene, implicated in increased risk of obesity, the leptin and leptin receptor genes, the proopiomelanocortin gene, and the brain-derived neurotrophic factor gene (Campbell et al. 2011). Heightened activity of the FTO gene, for example, may increase DNA methylation of genes involving resting energy expenditure. Individuals with two copies of a common polymorphism of the FTO gene are at increased risk of clinical obesity (Campbell et al. 2011). Researchers have looked at polymorphisms in the FTO gene to see if these correlated with eating disordered behaviors and thus far have not found this to be the case, rather the FTO gene is thought to influence energy metabolism or modulate the effects of energy expenditure (Jonassaint et al. 2011).
Associations between FTO rs9939609 polymorphism, serum vitamin D, mental health, and eating behaviors in overweight adults
Published in Nutritional Neuroscience, 2022
Mahsa Mehrdad, Mohammad Hassan Eftekhari, Fatemeh Jafari, Hossein-Ali Nikbakht, Maryam Gholamalizadeh
The worldwide prevalence of obesity is dramatically causing major health concerns [1]. Obesity is a complicated disorder caused by the interactions between genetic and environmental factors [2,3]. Some studies suggested that genetic factors are responsible for an estimated heritability of 40–70% for obesity and other diseases [4–6]. Several genome-wide association studies (GWASs) identified at least 75 genetic loci for obesity and its related traits [7]. The Fat Mass And Obesity-Associated (FTO) gene is recognized as the strongest genetic factor contributing to obesity [7–9]. The FTO rs9939609 polymorphism (NM_001080432.3:c.46-23525T > A) is the most common and strong variant in association studies on obesity [10,11]. This SNP is located within the first intron of the FTO gene and is associated with a higher body mass index (BMI), weight, fat mass, energy intake, as well as appetite regulation [12–14]. The GWASs with a large sample size of more than 90,000 subjects showed that this SNP could provide an explanation for 0.34% of BMI variance [15]. This extensively studied SNP was confirmed to have an association with the neural substrate activity associated with food-cue reactivity [16,17]. It is known that the FTO gene is expressed in all body tissues, and the highest expression is in the brain, especially in the hypothalamus, which regulates energy homeostasis, eating behavior, and appetite [10,18,19].
Effect of MTHFR (rs1801133) and FTO (rs9939609) genetic polymorphisms and obesity in T2DM: a study among Bengalee Hindu caste population of West Bengal, India
Published in Annals of Human Biology, 2021
Pranabesh Sarkar, Diptendu Chatterjee, Arup Ratan Bandyopadhyay
Another diabetes susceptibility gene that mediates its effect through obesity is FTO (fat mass and obesity associated gene) (Chauhan et al. 2011). It encodes 2-oxoglutarate-dependent nucleic acid demethylase that is involved in DNA repair and fatty acid metabolism and expressed in many metabolic disease-related tissues. FTO gene regulates the transcription of genes involved in fatty acid and glucose metabolism (Al-Tuma and Obed 2018). The association between A allele of FTO rs9939609 genetic polymorphism with T2DM and obesity has been reported in Finnish people (Qi et al. 2008; Legry et al. 2009). In contrast, FTO rs9939609 genetic polymorphism has not been associated with T2DM and obesity in Chinese Han or an African-American population and this might be due to the evolutionary divergence, genetic drift and lower A allele frequency (0.20) of FTO rs9939609 compared to Europeans (0.40) (Yajnik et al. 2009).
Effect of FTO and IGF2BP2 gene polymorphisms on duration of pregnancy and Apgar scores in women with gestational diabetes
Published in Journal of Obstetrics and Gynaecology, 2019
Maciej Tarnowski, Joanna Bujak, Patrycja Kopytko, Sandra Majcher, Przemysław Ustianowski, Violetta Dziedziejko, Krzysztof Safranow, Andrzej Pawlik
Other studies suggest that FTO gene polymorphism may be associated with the clinical parameters in newborns. Gesteiro et al. have indicated that FTO gene polymorphism may affect the insulin sensitivity and lipoprotein profiles in newborns (Gesteiro et al. 2016). Barton et al. suggest that the FTO gene polymorphism and placental FTO expression have been linked with foetal growth trajectories (Barton et al. 2016). In a study by Andraweera et al., FTO gene polymorphism was associated with being small-for-gestational-age and a spontaneous preterm birth (Andraweera et al. 2016). No association was found between the FTO gene polymorphism and a newborn weight status in a Brazilian population (Kroll et al. 2017).