ArticleBMC medical genetics2009
Gastric inhibitory polypeptide receptor: association analyses for obesity of several polymorphisms in large study groups.
Article in BMC medical genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 30 citations in OpenAlex.
- Molecular impact of single nucleotide polymorphisms in GIPR gene among type 2 diabetes mellitus patients in the Saudi population.Diabetology & metabolic syndrome · 2025Article
- Sweet Taste Receptors' Genetic Variability in Advanced Potential Targets of Obesity.Nutrients · 2025Article
- Review
- Pharmacological Advances in Incretin-Based Polyagonism: What We Know and What We Don't.Physiology (Bethesda, Md.) · 2024Review
- Tirzepatide, GIP(1-42) and GIP(1-30) display unique signaling profiles at two common GIP receptor variants, E354 and Q354.Frontiers in pharmacology · 2024Article
- Genetic Variability of Incretin Receptors and Alcohol Dependence: A Pilot Study.Frontiers in molecular neuroscience · 2022Article
- Loss of Function Glucose-Dependent Insulinotropic Polypeptide Receptor Variants Are Associated With Alterations in BMI, Bone Strength and Cardiovascular Outcomes.Frontiers in cell and developmental biology · 2021Article
- Genome-wide association study of alcohol dependence implicates a region on chromosome 11.Alcoholism, clinical and experimental research · 2010Article
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Authors and funding
16 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGastric inhibitory polypeptide (GIP) is postulated to be involved in type 2 diabetes mellitus and obesity. It exerts its function through its receptor, GIPR. We genotyped three GIPR SNPs (rs8111428, rs2302382 and rs1800437) in German families with at least one obese index patient, two case-control studies and two cross-sectional population-based studies.
methodsGenotyping was performed by MALDI-TOF, ARMS-PCR and RFLP. The family-study: 761 German families with at least one extremely obese child or adolescent (n = 1,041) and both parents (n = 1,522). Case-control study: (a) German obese children (n = 333) and (b) obese adults (n = 987) in comparison to 588 adult lean controls. The two cross-sectional population-based studies: KORA (n = 8,269) and SHIP (n = 4,310).
resultsWe detected over-transmission of the A-allele of rs2302382 in the German families (pTDT-Test = 0.0089). In the combined case-control sample, we estimated an odd ratio of 1.54 (95%CI 1.09;2.19, pCA-Test = 0.014) for homozygotes of the rs2302382 A-allele compared to individuals with no A-allele. A similar trend was found in KORA where the rs2302382 A-allele led to an increase of 0.12 BMI units (p = 0.136). In SHIP, however, the A-allele of rs2302382 was estimated to contribute an average decrease of 0.27 BMI units (p-value = 0.031).
conclusionOur data suggest a potential relevance of GIPR variants for obesity. However, additional studies are warranted in light of the conflicting results obtained in one of the two population-based studies.
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