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Obesity genes

obesity

By Li Dali, Ph.D.

If you tested your DNA with a personal genomics service like 23andMe, AncestryDNA, FamilyTreeDNA, MyHeritage or another testing company, you can learn more about your risk factors for hundreds of diseases. By clicking the button above ⬆️, you can upload your raw DNA data file and receive a personalized 250-page health report with research links that is the most comprehensive.

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:

rs1421085Variation in the FTO gene contributes to obesity in children and severe obesity in adults.
rs1558902Variants 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.
rs1528133TUB gene polymorphisms are a candidate for late-life obesity in women.
rs2272382TUB gene polymorphisms are a candidate for late-life obesity in women.
rs2272383TUB gene polymorphisms are a candidate for late-life obesity in women.
rs16953002There is a 1.32-fold increased risk of melanoma in people with a low BMI.
rs17782313The 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.
rs17817449The FTO genetic variant affects obesity, insulin sensitivity, leptin levels and resting metabolic rate.
rs9939609The 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.
rs987237The AA genotype of the TFAP2B gene was associated with greater weight loss on a low-fat, high-protein diet.
rs1121980SNP rs1121980 in the FTO gene showed the strongest association with obesity risk (2.76-fold increase).
rs8050136Obesity-related heterogeneity in models of predisposition to type 2 diabetes.
rs4994A 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

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.

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