LEPR rs1137102: What Your Genotype Means
The rs1137102 single nucleotide polymorphism is a missense variant located within the leptin receptor (LEPR) gene, altering codon 656 from lysine to asparagine (Lys656Asn). It has been studied extensively for its potential influence on receptor signaling efficiency and adiposity-related traits. However, large-scale meta-analyses demonstrate that evidence connecting this specific variant directly to body mass index or overweight risk remains limited and inconsistent.
What each genotype means
Typical receptor signaling
This genotype represents the common form of the LEPR gene at this position. Research into this variant (p.Lys656Asn) suggests that individuals with this profile do not carry the specific amino acid change associated with altered leptin receptor signaling efficiency. This is considered the baseline state in most population studies.
This is the most common genotype in most global populations, carried by the majority of individuals.
Potential signaling variation
You carry one copy of the variant allele, which results in a Lysine to Asparagine change (p.Lys656Asn) in the leptin receptor. Epidemiological studies have investigated whether this change influences receptor signaling and body weight regulation, though evidence remains limited and inconsistent across different ethnic groups. It is not a diagnostic marker for obesity or metabolic disease.
This heterozygous genotype is found in approximately 25-40% of individuals in many European and American populations.
Variant receptor signaling
You carry two copies of the variant allele, which results in the p.Lys656Asn change in the leptin receptor. Some research suggests this variant may be linked to differential signaling efficiency and adiposity traits, but findings are mixed and often show weak or no significant association in large-scale studies. This genotype does not determine your health outcomes and should be viewed in the context of your overall lifestyle and genetic background.
This homozygous variant genotype is less common, typically observed in roughly 5-10% of individuals in European and American populations.
Molecular Anatomy and the LEPR Gene
Single nucleotide polymorphism rs1137102 is an exonic missense variation residing on chromosome 1 within the leptin receptor (LEPR) gene. At the nucleotide level, the variant typically involves a G to C exchange (or G to T/C depending on transcript orientation and reporting conventions), resulting in the substitution of lysine with asparagine at amino acid position 656 (p.Lys656Asn). This alteration lies within the extracellular domain of the leptin receptor, a region fundamental for ligand engagement and signal transduction. The LEPR protein is expressed predominantly in the central nervous system, particularly the hypothalamus, as well as in peripheral metabolic tissues. Under standard physiological conditions, the binding of leptin to its receptor initiates downstream signaling cascades, including the JAK-STAT pathway, which govern energy homeostasis, appetite suppression, and neuroendocrine function. Researchers initially hypothesized that structural alterations in the extracellular domain could alter leptin binding kinetics or receptor expression at the cell surface, potentially modulating physiological satiety.
Evidence from Epidemiological and Metabolic Studies
Because of leptin's essential role in metabolism, early candidate gene investigations hypothesized that rs1137102 might significantly influence susceptibility to obesity, fat distribution, or metabolic syndrome. Some initial candidate studies noted modest variations in circulating leptin concentrations, blood pressure, or body composition among individuals carrying different genotypes. However, systematic reviews and meta-analyses, such as broad evaluations across population cohorts like the CoLaus study, have largely demonstrated no robust, generalizable association between rs1137102 and overweight or elevated body mass index. In broader genome-wide association studies (GWAS) measuring adiposity traits, rs1137102 rarely meets stringent significance thresholds independently. The scientific evidence regarding direct phenotypic effects is classified as limited, with several researchers noting that earlier positive findings may have been confounded by population stratification, modest sample sizes, or complex gene-environment interactions that do not replicate across broader cohorts.
Population Distribution and Evolutionary Context
The frequency of rs1137102 alleles varies substantially among major global populations. In European and American cohorts, the minor allele (frequently annotated as the 656Asn or C allele) exhibits an estimated frequency between 0.15 and 0.25, indicating that heterozygous carriers are relatively common in these groups. Conversely, evolutionary genomic surveys have documented marked differences across other continental ancestries. In East Asian populations, the derived allele frequency is markedly lower, with evidence from selection scans suggesting ancient evolutionary pressures and natural selection operating differently across ancestral geographic regions. Because baseline allele frequencies naturally shift along geographic clines, geneticists emphasize that association studies must rigorously correct for ancestral backgrounds to avoid spurious correlations between normal population variation and complex polygenic traits.
Practical Implications and Limitations
Understanding your rs1137102 genotype provides an interesting glimpse into normal human genetic diversity, but it cannot be used as a clinical diagnostic tool or a standalone predictor of your metabolic health. Body mass index, fat distribution, and metabolic traits are highly polygenic, shaped by the combined action of hundreds of subtle genetic variants alongside daily lifestyle, nutrition, sleep quality, and physical activity. Carrying a variant allele at rs1137102 does not mean an individual is destined to experience weight challenges, nor does having the ancestral genotype confer immunity against metabolic conditions. For questions regarding metabolic health or weight management, evidence-based lifestyle choices and consultations with primary healthcare providers remain the primary determinants of clinical outcomes.
How common is this variant?
The minor allele frequency of rs1137102 ranges between approximately 0.15 and 0.25 in European and American populations, while it is observed at substantially lower frequencies in East Asian cohorts.
Frequently asked questions
Does having the LEPR rs1137102 variant cause obesity?
No, carrying the rs1137102 variant does not cause obesity. While candidate gene studies explored its potential role in body mass, large systematic reviews have confirmed that it does not show a reliable, independent link to overweight status.
Can rs1137102 predict how hungry I feel or my leptin levels?
Scientific research does not support using rs1137102 to predict personal appetite, satiety, or circulating leptin levels. Regulating appetite is a complex biological process influenced by numerous hormones, neuroendocrine circuits, and diet rather than a single common genetic marker.
Is LEPR rs1137102 considered a medical diagnosis?
No, rs1137102 is a common benign polymorphism and is not a clinical or medical diagnosis. It does not indicate the presence of monogenic leptin receptor deficiency, which is caused by rare loss-of-function mutations.
Should I change my diet or exercise routine based on this genotype?
You should not alter your nutritional or exercise habits solely based on your rs1137102 genotype. Consistent lifestyle fundamentals, including balanced nutrition and routine physical activity, remain the standard guidance regardless of your genetic variation at this site.
Sources & further reading
Educational information only, last refreshed 9/8/2026. Not medical advice — these associations describe population statistics, not individual predictions.
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This SNP is associated with leptin receptor function and regulation of appetite.
A variant in the leptin receptor gene associated with altered satiety signaling and potential predisposition to obesity.
Common missense variant (Lys656Asn) in the leptin receptor associated with altered body mass index, insulin resistance, and metabolic traits.