rs10423928 - GIPR

Magnitude 2.2 · 8 studies on file

Reported associations

• Genetic variants associated with glycemic response to treatment with dipeptidylpeptidase 4 inhibitors. - Pharmacogenomics (2023) · Űrgeová A, Javorský M, Klimčáková L, Židzik J, Šalagovič J, Hubáček JA, Doubravová P, Gotthardová I, Kvapil M, Pelikánová T, Tkáč I, Yaluri AS · PubMed 32308134

  We examined associations of eight SNPs in/near seven candidate genes with glycemic response to 6 month treatment with DPP4 inhibitors. 206 patients with type 2 diabetes (116 men and 90 women) were treated with sitagliptin or vildagliptin (both 100 mg/day) in combination with metformin or metformin/sulphonylurea over 6 months, and the reduction in glycated hemoglobin (HbA ) was measured. Rs6923761 in was significantly associated with a reduction in HbA (adjusted p = 0.006). Homozygotes for the minor A allele had smaller reduction in HbA by 0.4% (4 mmol/mol) than the G allele carriers (p = 0.016). The missense variant rs6923761 in the gene was associated with a smaller glycemic response to 6 month gliptin therapy in diabetic patients of central European origin.

• Body surface area is a potential obesity index: Its genetic determination and its causality for later-life diseases. - Obesity (Silver Spring, Md.) (2022) · Yu XH, Cao RR, Yang YQ, Deng FY, Bo L, Lei SF · PubMed 36502284

  This study aimed to identify novel genetic factors that contribute to body surface area (BSA) and explore its relationship with complex traits and diseases. Based on more than 330,000 European individuals in the UK Biobank, the first large-scale genome-wide association study for BSA was performed. Comprehensive genetic analysis and enrichment analysis were then performed to explore the biological function of the identified loci. The genetic correlations and causal associations between BSA and other anthropometry parameters, early growth indices, and later-life diseases, respectively, were assessed by complex genetic approaches. Genome-wide association study analysis identified a total of 456 conditionally independent single-nucleotide polymorphism mapping genes with known functions in the

• Leveraging Polygenic Functional Enrichment to Improve GWAS Power. - American journal of human genetics (2019) · Kichaev G, Bhatia G, Loh PR, Gazal S, Burch K, Freund MK, Schoech A, Pasaniuc B, Price AL · PubMed 30595370

  Functional genomics data has the potential to increase GWAS power by identifying SNPs that have a higher prior probability of association. Here, we introduce a method that leverages polygenic functional enrichment to incorporate coding, conserved, regulatory, and LD-related genomic annotations into association analyses. We show via simulations with real genotypes that the method, functionally informed novel discovery of risk loci (FINDOR), correctly controls the false-positive rate at null loci and attains a 9%-38% increase in the number of independent associations detected at causal loci, depending on trait polygenicity and sample size. We applied FINDOR to 27 independent complex traits and diseases from the interim UK Biobank release (average N = 130K). Averaged across traits, we attaine

• Genetic analysis of quantitative traits in the Japanese population links cell types to complex human diseases. - Nature genetics (2019) · Kanai M, Akiyama M, Takahashi A, Matoba N, Momozawa Y, Ikeda M, Iwata N, Ikegawa S, Hirata M, Matsuda K, Kubo M, Okada Y, Kamatani Y · PubMed 29403010

  Clinical measurements can be viewed as useful intermediate phenotypes to promote understanding of complex human diseases. To acquire comprehensive insights into the underlying genetics, here we conducted a genome-wide association study (GWAS) of 58 quantitative traits in 162,255 Japanese individuals. Overall, we identified 1,407 trait-associated loci (P < 5.0 × 10 ), 679 of which were novel. By incorporating 32 additional GWAS results for complex diseases and traits in Japanese individuals, we further highlighted pleiotropy, genetic correlations, and cell-type specificity across quantitative traits and diseases, which substantially expands the current understanding of the associated genetics and biology. This study identified both shared polygenic effects and cell-type specificity

• Contribution of genetics to visceral adiposity and its relation to cardiovascular and metabolic disease. - Nature medicine (2019) · Karlsson T, Rask-Andersen M, Pan G, Höglund J, Wadelius C, Ek WE, Johansson Å · PubMed 31501611

  Visceral adipose tissue (VAT)-fat stored around the internal organs-has been suggested as an independent risk factor for cardiovascular and metabolic disease , as well as all-cause, cardiovascular-specific and cancer-specific mortality . Yet, the contribution of genetics to VAT, as well as its disease-related effects, are largely unexplored due to the requirement for advanced imaging technologies to accurately measure VAT. Here, we develop sex-stratified, nonlinear prediction models (coefficient of determination = 0.76; typical 95% confidence interval (CI) = 0.74-0.78) for VAT mass using the UK Biobank cohort. We performed a genome-wide association study for predicted VAT mass and identified 102 novel visceral adiposity loci. Predicted VAT mass was associated with increased risk

• A missense variant in GLP1R gene is associated with the glycaemic response to treatment with gliptins. - Diabetes, obesity & metabolism (2017) · Javorský M, Gotthardová I, Klimčáková L, Kvapil M, Židzik J, Schroner Z, Doubravová P, Gala I, Dravecká I, Tkáč I · PubMed 27160388

  Gliptins act by increasing endogenous incretin levels. Glucagon-like peptide-1 receptor (GLP1R) and glucose-dependent insulinotropic peptide receptor (GIPR) are their indirect drug targets. Variants of GLP1R and GIPR have previously been associated with the incretin effect. The aim of the present pilot study was to examine associations of the GLP1R and GIPR gene variants with the glycaemic response to gliptins. A total of 140 consecutive patients with type 2 diabetes were followed-up 6 months after initiation of gliptin treatment. GLP1R rs6923761 (Gly168Ser) and GIPR rs10423928 genotyping was performed using real-time PCR, with subsequent high-resolution melting analysis. The main study outcome was reduction in glycated haemoglobin (HbA1c) after treatment. GLP1R Gly168Ser variant was sig

• GIPR Gene Polymorphism and Weight Gain in Patients With Schizophrenia Treated With Olanzapine. - The Journal of neuropsychiatry and clinical neurosciences (2016) · Ono S, Suzuki Y, Fukui N, Sawamura K, Sugai T, Watanabe J, Tsuneyama N, Someya T · PubMed 25321336

  Association between gastric inhibitory polypeptide receptor polymorphism, rs10423928, and body mass index in olanzapine-treated schizophrenia was examined. Body mass index change for the A/T+A/A genotypes was significantly higher than that for the T/T genotype. rs10423928 may predict weight gain in schizophrenia.

• Association between the GIPR gene and the insulin level after glucose loading in schizophrenia patients treated with olanzapine. - The pharmacogenomics journal (2013) · Ono S, Suzuki Y, Fukui N, Sugai T, Watanabe J, Tsuneyama N, Someya T · PubMed 21747410

  Several studies have shown increased rates of hyperglycemia and diabetes in schizophrenic patients treated with olanzapine. However, the underlying mechanism is poorly understood. Glucose-dependent insulinotropic polypeptide (GIP) is known to affect insulin secretion by pancreatic β cells. Recently, a meta-analysis study reported an association between a GIP receptor (GIPR) gene polymorphism (rs10423928) and insulin secretion measured by an oral glucose tolerance test (OGTT). We assessed the influence of this GIPR gene polymorphism on glucose metabolism in 60 schizophrenic patients treated with olanzapine and 103 healthy controls. The GIPR gene polymorphism was determined using TaqMan methods. We performed repeated-measures analysis of variance (ANOVA) and one-way ANOVA for the glucose an

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