What you carry at this position in your DNA and what research says about it.
Obesity and Weight Gain: 10/10 evidence, 51 publications.
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Sample genotype (not yours): T/T
Typical Obesity Risk and Normal Fat Burning
Two copies of the T allele are associated with a typical body mass index and normal metabolic rate. Your fat cells are programmed to efficiently burn off excess energy as heat.
What this genotype means: Normal mitochondrial thermogenesis; Typical body mass index; Typical metabolic rate.
Sample genotype (not yours): C/C
Higher Risk of Obesity and Weight Gain
Two copies of the C allele are associated with a higher average body mass index and increased fat accumulation. Your fat cells are genetically programmed to store energy rather than burn it as heat.
What this genotype means: Significantly reduced mitochondrial thermogenesis; Higher average body mass index; Elevated risk of type 2 diabetes.
Sample genotype (not yours): T/C
Slightly Higher Risk of Obesity and Weight Gain
One copy of the C allele is linked to a slightly higher body mass index and a tendency to store more fat. Your fat cells may have a slightly reduced capacity to burn off excess energy as heat.
What this genotype means: Slightly reduced mitochondrial thermogenesis; Slightly higher average body mass index; Modestly increased risk of type 2 diabetes.
Gene function and biological role
Gene Function: The FTO gene encodes an enzyme that plays a critical role in regulating energy balance and body fat accumulation [1]. It is highly expressed in the brain's hypothalamus, which controls appetite, as well as in peripheral fat tissues [1]. Although originally named fat mass and obesity-associated gene, its exact molecular targets in metabolic regulation have been a major focus of genetic research [2]. Studies show that FTO influences how the body decides to store energy as fat or burn it off as heat [2]. This gene represents the strongest genetic link to common obesity discovered to date [1].
Variant Impact: The rs1421085 variant is located within the first intron of the FTO gene and acts as a major regulatory switch [2]. The T-to-C change disrupts a binding site for a repressor protein called ARID5B [2]. Without this repressor, two downstream genes, IRX3 and IRX5, become highly active during early fat cell development [2]. This molecular shift prevents fat cells from developing into energy-burning beige fat, forcing them to become energy-storing white fat instead [2]. Consequently, this single-letter change reduces mitochondrial heat production and increases lipid accumulation [2].
Key Insight: This variant does not change the FTO protein itself, but acts as a genetic switch that alters how fat cells burn energy.
Location: FTO. Chromosome 16 · 16q12.2 · 53.8 Mb
Estimated prevalence by population
Global 49.9%; European 34.0%; African 80.6%; East Asian 71.6%; South Asian 44.7%; Americas 50.6%; Ashkenazi 23.9%; Finnish 33.3%; Middle Eastern 38.3%; Amish 26.0%.
Estimated TT genotype frequency.
Global 38.6%; European 48.6%; African 18.3%; East Asian 26.1%; South Asian 44.3%; Americas 41.1%; Ashkenazi 50.0%; Finnish 48.8%; Middle Eastern 47.2%; Amish 50.0%.
Estimated TC genotype frequency.
Global 11.5%; European 17.4%; African 1.0%; East Asian 2.4%; South Asian 11.0%; Americas 8.3%; Ashkenazi 26.1%; Finnish 17.9%; Middle Eastern 14.5%; Amish 24.0%.
Estimated CC genotype frequency.
Showing effects for T/T genotype
Cardiovascular & Metabolic
Obesity & Body Composition
Obesity. Evidence: 10/10. Source: PMID 19151714. Typical Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 26604143. Typical BMI.
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Typical Fat %.
Diabetes & Glycemic Traits
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. Typical Risk.
Endocrine & Reproductive
Pregnancy & Birth Complications
Preeclampsia. Evidence: 8/10. Source: PMID 33239696. Typical Risk.
Showing effects for C/C genotype
Obesity. Evidence: 10/10. Source: PMID 19151714. Higher Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 26604143. Higher BMI.
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Higher Fat %.
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. Higher Risk.
Preeclampsia. Evidence: 8/10. Source: PMID 33239696. Higher Risk.
Showing effects for T/C genotype
Obesity. Evidence: 10/10. Source: PMID 19151714. Slightly Higher Risk.
Body Mass Index. Evidence: 10/10. Source: PMID 26604143. Slightly Higher BMI.
Body Fat Percentage. Evidence: 10/10. Source: PMID 30593698. Slightly Higher Fat %.
Type 2 Diabetes. Evidence: 10/10. Source: PMID 32541925. Slightly Higher Risk.
Preeclampsia. Evidence: 8/10. Source: PMID 33239696. Slightly Higher Risk.
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Two copies of the protective T allele mean you carry a genetic profile that supports normal metabolic function [1]. This genetic setup allows a repressor protein to bind normally, keeping downstream genes quiet during fat cell development [2]. As a result, your preadipocytes can successfully mature into energy-burning beige fat cells rather than energy-storing white fat cells [2]. This process, known as thermogenesis, helps your body dissipate excess calories as heat instead of storing them as fat [2]. Population studies consistently show that individuals with this genotype have a lower average body mass index and a reduced risk of obesity compared to those with the C allele [1]. They also exhibit a lower risk of developing type 2 diabetes and related metabolic complications [3]. Maintaining a balanced diet and regular physical activity remains key to supporting your natural metabolic efficiency.
Normal mitochondrial thermogenesis; Typical body mass index; Typical metabolic rate.
Sample genotype: CC (Homozygous)
Two copies of the FTO risk allele represent the strongest common genetic risk factor for obesity [1]. This genetic profile fully disrupts the binding of the ARID5B repressor protein during fat cell development [2]. Without this repressor, the IRX3 and IRX5 genes are highly active, causing a major developmental shift in your fat tissue [2]. Instead of forming energy-burning beige fat cells, your body preferentially develops energy-storing white fat cells [2]. This significantly reduces mitochondrial thermogenesis, meaning your body burns fewer calories as heat and stores more as lipid droplets [2]. Clinical and epidemiological studies show that individuals with the C/C genotype have a significantly higher average body weight and body fat percentage [3]. They also face an elevated risk of metabolic conditions, including type 2 diabetes and preeclampsia [4] [5]. While this genetic predisposition is strong, lifestyle interventions like regular exercise and a balanced diet remain highly effective at managing weight.
Significantly reduced mitochondrial thermogenesis; Higher average body mass index; Elevated risk of type 2 diabetes.
Sample genotype: TC (Heterozygous)
One copy of the obesity-associated C allele means you carry a genetic variant that can influence how your body stores fat [1]. This single-letter change partially disrupts the binding of a key repressor protein in your preadipocytes [2]. Consequently, downstream genes that promote fat storage are slightly more active, shifting some fat cells from energy-burning beige fat to energy-storing white fat [2]. This molecular shift can slightly lower your body's rate of thermogenesis, making it easier to store excess calories as fat [2]. Large-scale genetic studies show that carriers of one C allele have a slightly higher average body mass index and body fat percentage [3]. This genotype is also associated with a modest increase in the risk of developing type 2 diabetes [4]. Engaging in regular cardiovascular exercise and eating a fiber-rich diet can help counteract this genetic tendency by promoting metabolic health.
Slightly reduced mitochondrial thermogenesis; Slightly higher average body mass index; Modestly increased risk of type 2 diabetes.
Variants with shared genetic architecture
rs11075995 · FTO Gene · Chr 16 · Breast Cancer Risk
rs11642015 · FTO Gene · Chr 16 · Weight and Diabetes Risk
rs8050136 · FTO Gene · Chr 16 · Weight and Diabetes Risk
Variation in FTO contributes to childhood obesity and severe adult obesity.
FTO Obesity Variant Circuitry and Adipocyte Browning in Humans.
Leveraging Polygenic Functional Enrichment to Improve GWAS Power.
Content updated August 2026.
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