← Back to Knowledge Base

Primary topic: LEPR leptin resistance gene

LEPR Gene and Metabolism: What It Means for Your Body

LEPR becomes relevant when satiety signals feel unreliable and weight regulation seems harder than generic advice would predict.

What is the LEPR gene?

LEPR encodes the leptin receptor, which helps the brain interpret energy-availability and satiety signals. It is part of the system that decides whether appetite should settle down after sufficient intake.

How LEPR affects metabolism

If LEPR-related signaling is weaker, satiety cues may feel less reliable. That can make weight regulation harder because appetite pressure stays stronger than expected.

What happens when LEPR is altered

Altered LEPR function does not guarantee leptin resistance, but it can raise the odds that appetite regulation deserves more structured follow-up.

Curated SNP evidence for LEPR

These SNPs come from the approved study-level evidence model. Each claim is scored from curated study rows, then gated before it can influence pathway scoring.

Glucose

Evidence-backed report connection

LEPR currently has 2 curated SNPs, 6 claim-level scores, and 0 claims eligible for pathway scoring.

Open the sample report
rs1137100K109R3 claims · 9 study rows

unknown · AA

LEPR unscored target

Not used for pathway scoring

rs1137100 AA has no scored directional claim for LEPR unscored target.

LEPR rs1137100 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137100 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.326A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR K109R, rs1137100, and Q223R, rs1137101, for type 2 diabetes risk. For K109R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137100 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.

unknown · AG

LEPR unscored target

Not used for pathway scoring

rs1137100 AG has no scored directional claim for LEPR unscored target.

LEPR rs1137100 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137100 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.326A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR K109R, rs1137100, and Q223R, rs1137101, for type 2 diabetes risk. For K109R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137100 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.

unknown · GG

LEPR unscored target

Not used for pathway scoring

rs1137100 GG has no scored directional claim for LEPR unscored target.

LEPR rs1137100 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137100 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.326A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR K109R, rs1137100, and Q223R, rs1137101, for type 2 diabetes risk. For K109R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137100 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.
rs1137101Q223R3 claims · 9 study rows

unknown · AA

LEPR unscored target

Not used for pathway scoring

rs1137101 AA has no scored directional claim for LEPR unscored target.

LEPR rs1137101 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137101 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.668A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR Q223R, rs1137101, and K109R, rs1137100, for type 2 diabetes risk. For Q223R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137101 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.

unknown · AG

LEPR unscored target

Not used for pathway scoring

rs1137101 AG has no scored directional claim for LEPR unscored target.

LEPR rs1137101 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137101 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.668A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR Q223R, rs1137101, and K109R, rs1137100, for type 2 diabetes risk. For Q223R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137101 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.

unknown · GG

LEPR unscored target

Not used for pathway scoring

rs1137101 GG has no scored directional claim for LEPR unscored target.

LEPR rs1137101 is treated as an unknown-effect coding variant with no scored genotype direction.

Likely effectNo clear DNA signal
Signal sizeMinimal signal
Evidence supportVery limited support
Report useEvidence only, not scored
Show study evidence
NCBI RefSNP recordidentity only · unknownNCBI RefSNP data identify rs1137101 as an LEPR coding variant with A and G alleles on the current RefSeq transcript, including NM_002303.6:c.668A>G among the annotated alleles. This supports using AA, AG, and GG genotype letters for the simplified record.PubMed 29293570review · loose proxyYang and Niu meta-analyzed LEPR Q223R, rs1137101, and K109R, rs1137100, for type 2 diabetes risk. For Q223R, the pooled allele and genotype models did not show a significant association after the authors' multiplicity threshold, and their bioinformatics analysis predicted the missense SNPs to be functionally neutral and benign. This supports leaving rs1137101 unscored for end-user genotype effect.PubMed 20874424biomarker association · loose proxySaukko et al. studied LEPR Lys109Arg and Gln223Arg in a middle-aged control population and reported some associations with cardiovascular risk-factor measures, but no leptin concentration differences between genotypes. This does not support a clear receptor-activity or biomarker direction for an individual end-user record.

Common symptoms people report

  • hunger that seems stronger than meal size would predict
  • difficulty feeling satisfied after standard meals
  • weight gain pressure that seems hard to explain
  • frustration with generic appetite-control advice

Biomarkers to validate

Fasting insulin

Useful because appetite and glucose regulation often overlap.

Triglycerides

Adds metabolic context when weight-regulation questions cluster.

Leptin when clinically relevant

Can provide extra context, though interpretation depends on the full picture.

Where DNA analysis helps

DNA helps identify whether satiety and leptin-related signaling should be one of the first systems you validate rather than treating appetite as a purely behavioral issue.

Example Insight

Your satiety-signaling pathway may create more pressure around food intake than standard diet advice assumes.

Suggested validation: fasting insulin and triglycerides.

What to do next

  • Check metabolic markers before treating appetite control as only a willpower problem.
  • Compare LEPR with FTO and IRS1 when weight and glucose issues overlap.
  • Use structured meal and biomarker context to test whether the pathway is relevant.

Upload your DNA file and receive a structured metabolic pathway analysis with prioritized insights and suggested validation markers.

Get My DNA Report

Related pages

FTO

FTO gene weight gain

IRS1

IRS1 insulin signaling gene

Triglycerides

triglycerides and metabolic health

Fasting insulin

fasting insulin and metabolism

Glucose regulation pathway

glucose regulation pathway

Lipid transport pathway

lipid transport pathway

Genetic test for weight loss Europe

genetic test for weight loss Europe

Related symptom angle

Why do I gain weight easily genetics

Browse the knowledge base

See the full index of gene guides, biomarker guides, pathway guides, symptoms, buyer pages, and common questions.