rs10925760 (KRT18P32): Plasma Metabolite GWAS
Key takeaways
- rs10925760 lies near two pseudogenes, KRT18P32 and MIPEPP2, and was identified in a GWAS of 217 plasma metabolites.
- The study enrolled 2,076 Framingham Heart Study participants and used a liquid chromatography-mass spectrometry platform.
- For most metabolites examined, inherited factors explained more individual variation than clinical factors like age, BMI, or blood pressure.
- The GWAS reported 31 metabolite-linked loci in total, 23 of which were novel at the time of publication.
Key takeaways
- rs10925760 lies near two pseudogenes, KRT18P32 (keratin 18 pseudogene 32) and MIPEPP2, and was flagged in a genome-wide study linking genetic variants to plasma metabolite levels.
- The identifying study measured 217 plasma metabolites in 2,076 Framingham Heart Study participants using a liquid chromatography-mass spectrometry (LC-MS) platform.
- For the majority of metabolites examined, inherited factors explained more than 20% of individual variation, often surpassing the combined effect of clinical factors such as age, BMI, and blood pressure.
- The GWAS identified 31 genetic loci tied to metabolite levels, 23 of which had not been previously reported at the time of publication.
What the research says rs10925760, located near the pseudogenes KRT18P32 (keratin 18 pseudogene 32, on the same genomic stretch as MIPEPP2), was identified in a genome-wide association study of 217 plasma metabolites measured in 2,076 participants from the Framingham Heart Study Offspring Cohort. The study used an LC-MS platform covering 113 polar analytes and 104 lipid analytes, including more than 100 metabolites not examined in prior comparable GWAS. Across the full panel, heritability exceeded 20% of inter-individual variation for the majority of analytes, and the analysis reported 31 loci associated with metabolite levels, 23 of which were novel.
Reported associations
- Plasma metabolite levels: The variant was among 31 genetic loci identified in a GWAS of 217 circulating metabolites in 2,076 Framingham Heart Study participants; the specific metabolite associated with this locus is not described in the available study text.
Evidence quality The available evidence comes from a single GWAS conducted in 2,076 individuals from the Framingham Heart Study Offspring Cohort, a family-based sample with comprehensive cardiometabolic phenotyping. The study deployed an LC-MS metabolomics platform covering 217 analytes. The specific p-value, effect size, and replication status for this locus individually are not reported in the available text excerpt. Independent replication in other populations is not described. The evidence for this specific variant should be treated as preliminary. No conflicting findings are noted in the provided study text.
Lifestyle considerations No lifestyle considerations on file for this variant.
Frequently asked questions
What is rs10925760?
rs10925760 is a genetic variant near two pseudogenes, KRT18P32 and MIPEPP2. It was flagged in a genome-wide association study that linked genetic variants to levels of metabolites measured in plasma samples from the Framingham Heart Study.
What is KRT18P32?
KRT18P32 is a pseudogene, a DNA sequence that resembles a functional gene - in this case keratin 18 - but does not produce a known working protein. It sits in the same genomic region as MIPEPP2.
What is a plasma metabolite GWAS?
A plasma metabolite genome-wide association study scans hundreds of thousands of genetic variants to find ones statistically linked to the levels of small molecules circulating in the blood. The Framingham Heart Study GWAS described here covered 217 such molecules using mass spectrometry.
How strong is the evidence for rs10925760?
The evidence is preliminary. It comes from a single study of 2,076 participants, and specific effect sizes and independent replication data for this particular locus are not available in the published excerpt.
Is rs10925760 linked to any disease?
No disease association is reported for this variant in the available study. The research focused on plasma metabolite levels as quantitative traits, not on disease outcomes.