Obesity genes
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Although physical inactivity and consuming energy-dense foods are commonly identified as the main culprits behind obesity and overweight, there exist additional factors such as hormonal and genetic factors that can heighten the likelihood of developing obesity.
The causes of obesity, including environmental and lifestyle factors, as well as genetic predisposition, have been extensively researched by scientists. Currently, significant attention is being paid to examining the interplay between genes and the environment, which may be responsible for the escalating prevalence of obesity across the globe.
Obesity-related genes have been identified through recent advancements in genetic testing. Causative genes for obesity include Leptin (LEP), the leptin receptor (LEPR), proopiomelanocortin (POMC), prohormone convertase 1 (PCSK1), the melanocortin 4 receptor (MC4R), single-minded homolog 1 (SIM1), brain-derived neurotrophic factor (BDNF), and the neurotrophic tyrosine kinase receptor type 2 gene (NTRK2).
White adipose tissue secretes a protein called Leptin, which is encoded by a gene on chromosome 7 in humans. Leptin has the ability to cross the blood-brain barrier and bind to the presynaptic GABAergic neurons of the hypothalamus. This results in a decrease in appetite and an increase in energy expenditure. The arcuate nucleus of the hypothalamus is where Leptin binds to its receptor and inhibits the neuropeptide Y (NPY)/agouti-related protein (AgRP) pathway.
The POMC gene, located on chromosome 2 in humans, plays a role in suppressing appetite. It affects the leptin-melanocortin system by producing ACTH and alpha-MSH, which are derived from the POMC protein. When there is a deficiency of POMC, these hormones are not produced, resulting in increased hunger, a decrease in resting metabolic rate, and severe obesity with red hair and pale skin.
Before advanced genetic testing and next generation sequencing (NGS), the melanocortin-4 receptor (MC4R) gene was found in approximately 4% of childhood obesity cases and is now recognized as the most frequently associated gene.
The discovery of FTO as the first obesity-susceptibility gene through GWAS in European patients with type 2 diabetes is significant. Multiple SNPs in the gene's first intron have been linked to type 2 diabetes, but this association disappears when BMI is taken into account. This suggests that FTO's effect on BMI mediates the association between FTO and type 2 diabetes. A study in Sardinian patients confirmed these findings, identifying rs9939609 and rs9930506 SNPs in FTO that are significantly associated with BMI. Other GWAS studies in European populations have also found SNPs in the same chromosomal location. Furthermore, three large studies conducted in Asian populations reported significant associations between FTO SNPs (rs9939609, rs17817449, rs12149832) and BMI.
Follow the link of the selected polymorphism to read a brief description of how the selected polymorphism affects Obesity and see a list of existing studies.
SNP polymorphisms related to the topic Obesity:
| rs1421085 | Variation in the FTO gene contributes to obesity in children and severe obesity in adults. |
| rs1558902 | Variants in the FTO gene are associated with increased body mass index, obesity and diabetes. A high-protein diet was more beneficial for people with risk allele A. These findings suggest significant genetic heterogeneity in weight loss in response to dietary interventions. |
| rs1528133 | TUB gene polymorphisms are a candidate for late-life obesity in women. |
| rs2272382 | TUB gene polymorphisms are a candidate for late-life obesity in women. |
| rs2272383 | TUB gene polymorphisms are a candidate for late-life obesity in women. |
| rs16953002 | There is a 1.32-fold increased risk of melanoma in people with a low BMI. |
| rs17782313 | The rs17782313 (C) alleles are associated with higher body mass index (BMI), with an even larger effect in children. The average increase in BMI is 0.44 units. |
| rs17817449 | The FTO genetic variant affects obesity, insulin sensitivity, leptin levels and resting metabolic rate. |
| rs9939609 | The common variant rs9939609 of the FTO gene, associated with fat mass and obesity, is associated with fat cell lipolysis as well as early onset of extreme obesity. Studies show that carriers of the risk allele A demonstrate significantly greater weight loss on a fat-restricted diet than non-carriers. |
| rs987237 | The AA genotype of the TFAP2B gene was associated with greater weight loss on a low-fat, high-protein diet. |
| rs1121980 | SNP rs1121980 in the FTO gene showed the strongest association with obesity risk (2.76-fold increase). |
| rs8050136 | Obesity-related heterogeneity in models of predisposition to type 2 diabetes. |
| rs4994 | A beta-3-adrenergic receptor mutation is associated with visceral obesity but lowers serum triglyceride levels. Carriers of the G allele necessarily need strength training to lose weight and keep the body in good shape. |
| rs1805081 | |
| rs4712652 | |
| rs734597 | |
| rs699363 | |
| rs970843 | |
| rs10401969 | |
| rs4823173 | |
| rs12145833 | |
| rs11127485 | |
| rs17150703 | |
| rs10105606 | |
| rs651821 | |
| rs972317 | |
| rs1808579 | |
| rs2605100 | |
| rs6429082 | |
| rs2943650 | |
| rs534870 | |
| rs9568856 | |
| rs9299 | |
| rs7132908 | |
| rs6567160 | |
| rs13130484 | |
| rs10182181 | |
| rs2030323 | |
| rs2112347 | |
| rs7498665 | |
| rs887912 | |
| rs2531995 | |
| rs9816226 | |
| rs7138803 | |
| rs7141420 | |
| rs1800437 | |
| rs10968576 | |
| rs7185735 | |
| rs2207139 | |
| rs10938397 | |
| rs10871777 | |
| rs2568958 | |
| rs13078807 | |
| rs11642841 | |
| rs9930506 | |
| rs9940128 | |
| rs12149832 | |
| rs8044769 | |
| rs3751812 | |
| rs6499662 | |
| rs6499640 | |
| rs8043757 | |
| rs1861868 | |
| rs34114122 | |
| rs11075990 | |
| rs5082 | |
| rs2229616 | |
| rs16964465 | |
| rs16964476 | |
| rs3764220 | |
| rs3865188 | |
| rs6971091 | |
| rs4142322 | |
| rs17573102 | |
| rs9028 | |
| rs7149926 | |
| rs11753543 | |
| rs9736016 | |
| rs7635777 | |
| rs9384860 | |
| rs2470315 | |
| rs6093921 | |
| rs2283208 | |
| rs6928576 | |
| rs10945918 | |
| rs6902153 | |
| rs12925846 | |
| rs10954428 | |
| rs10797020 | |
| rs1578761 | |
| rs10489833 | |
| rs11264997 | |
| rs12540206 | |
| rs975118 | |
| rs7512592 | |
| rs1873511 | |
| rs6697656 | |
| rs6963221 | |
| rs6679056 | |
| rs6976491 | |
| rs7800006 | |
| rs1776012 | |
| rs2173676 | |
| rs2060457 | |
| rs2948300 | |
| rs2953802 | |
| rs435581 | |
| rs666595 | |
| rs2241005 | |
| rs750456 | |
| rs12295638 | |
| rs1435703 | |
| rs6726292 | |
| rs2274459 | |
| rs999943 | |
| rs9941349 | |
| rs10433903 | |
| rs6110577 | |
| rs7603514 | |
| rs12635698 | |
| rs10999409 | |
| rs7474896 | |
| rs374748 | |
| rs11624704 | |
| rs17126232 | |
| rs16867321 | |
| rs11680012 | |
| rs17773430 | |
| rs12463617 | |
| rs1993709 | |
| rs1957894 | |
| rs11208659 | |
| rs11109072 | |
| rs3101336 | |
| rs16923476 | |
| rs17025867 | |
| rs3782724 | |
| rs2275848 | |
| rs1631486 | |
| rs12408810 | |
| rs476828 | |
| rs564343 | |
| rs1048466 | |
| rs9328321 | |
| rs1704198 | |
| rs988712 | |
| rs2116830 | |
| rs17700144 | |
| rs4756846 | |
| rs297325 | |
| rs1424233 | |
About The Author
Li Dali
Li Dali, a National Foundation for Outstanding Youth Fund recipient, is a researcher at the School of Life Sciences in East China Normal University. He earned his PhD in genetics from Hunan Normal University in 2007 and conducted collaborative research at Texas A&M University during his doctoral studies. Li Dali and his team have optimized and innovated gene editing technology, leading to the establishment of a world-class system for constructing gene editing disease models. It is beneficial to comprehend the genetic impact on the molecular mechanisms and pathways that... BRCA stands for "BReast CAncer gene" and refers to two distinct genes, BRCA1 and BRCA2, which have... The DNA Diet report is tailored to assist with weight management by offering personalized diet and...
