ArticleDiabetologia2015
Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data.
Article in Diabetologia, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Genetic architecture of oral glucose-stimulated insulin release provides biological insights into type 2 diabetes aetiology.Nature metabolism · 2024Article
- Screening of 31 genes involved in monogenic forms of obesity in 23 Pakistani probands with early-onset childhood obesity: a case report.BMC medical genetics · 2019Article
- Human pancreatic islet three-dimensional chromatin architecture provides insights into the genetics of type 2 diabetes.Nature genetics · 2019Article
- The Predictive Factors for Diabetic Remission in Chinese Patients with BMI > 30 kg/mObesity surgery · 2018Article
- Genetic Correlation between Body Fat Percentage and Cardiorespiratory Fitness Suggests Common Genetic Etiology.PloS one · 2016Article
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisWe examined the extent to which surrogate measures of insulin release have shared genetic causes.
methodsGenetic and phenotypic correlations were calculated in a family cohort (n = 315) in which beta cell indices were estimated based on fasting and oral glucose-stimulated plasma glucose, serum C-peptide and serum insulin levels. Furthermore, we genotyped a large population-based cohort (n = 6,269) for common genetic variants known to associate with type 2 diabetes, fasting plasma glucose levels or fasting serum insulin levels to examine their association with various indices.
resultsWe found a notable difference between the phenotypic and genetic correlations for the traits, emphasising that the phenotypic correlation is an insufficient measure of the magnitude of shared genetic impact. In addition, we found that corrected insulin response, insulinogenic index and incAUC for insulin after an oral glucose challenge shared the majority of their genetic backgrounds, with genetic correlations of 0.80-0.99. The BIGTT index for acute insulin response differed slightly more from the latter with genetic correlations of 0.78-0.87. The HOMA for beta cell function was genetically closely related to fasting insulin with a genetic correlation of 0.85. The effects of 82 selected susceptibility single nucleotide polymorphisms on these insulin secretion indices supported our interpretation of the data and added insight into the biological differences between the examined traits. CONCLUSIONS/
interpretationThe level of shared genetic background varies between surrogate measures of insulin release, and this should be considered when designing a genetic association study to best obtain information on various mechanisms of insulin release.
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Registered trials
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