Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data

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Standard

Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data. / Gjesing, Anette Marianne Prior; Ribel-Madsen, Rasmus; Harder, Marie Neergaard; Eiberg, Hans; Grarup, Niels; Jørgensen, Torben; Ekstrøm, Claus T; Pedersen, Oluf; Hansen, Torben.

In: Diabetologia, Vol. 58, No. 5, 05.2015, p. 1006-1012.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Gjesing, AMP, Ribel-Madsen, R, Harder, MN, Eiberg, H, Grarup, N, Jørgensen, T, Ekstrøm, CT, Pedersen, O & Hansen, T 2015, 'Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data', Diabetologia, vol. 58, no. 5, pp. 1006-1012. https://doi.org/10.1007/s00125-015-3516-9

APA

Gjesing, A. M. P., Ribel-Madsen, R., Harder, M. N., Eiberg, H., Grarup, N., Jørgensen, T., Ekstrøm, C. T., Pedersen, O., & Hansen, T. (2015). Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data. Diabetologia, 58(5), 1006-1012. https://doi.org/10.1007/s00125-015-3516-9

Vancouver

Gjesing AMP, Ribel-Madsen R, Harder MN, Eiberg H, Grarup N, Jørgensen T et al. Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data. Diabetologia. 2015 May;58(5):1006-1012. https://doi.org/10.1007/s00125-015-3516-9

Author

Gjesing, Anette Marianne Prior ; Ribel-Madsen, Rasmus ; Harder, Marie Neergaard ; Eiberg, Hans ; Grarup, Niels ; Jørgensen, Torben ; Ekstrøm, Claus T ; Pedersen, Oluf ; Hansen, Torben. / Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data. In: Diabetologia. 2015 ; Vol. 58, No. 5. pp. 1006-1012.

Bibtex

@article{3c8850145ea64f1795f506e67d3044c5,
title = "Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data",
abstract = "AIMS/HYPOTHESIS: We examined the extent to which surrogate measures of insulin release have shared genetic causes.METHODS: Genetic 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.RESULTS: We 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/INTERPRETATION: The 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.",
author = "Gjesing, {Anette Marianne Prior} and Rasmus Ribel-Madsen and Harder, {Marie Neergaard} and Hans Eiberg and Niels Grarup and Torben J{\o}rgensen and Ekstr{\o}m, {Claus T} and Oluf Pedersen and Torben Hansen",
year = "2015",
month = may,
doi = "10.1007/s00125-015-3516-9",
language = "English",
volume = "58",
pages = "1006--1012",
journal = "Diabetologia",
issn = "0012-186X",
publisher = "Springer",
number = "5",

}

RIS

TY - JOUR

T1 - Genetic and phenotypic correlations between surrogate measures of insulin release obtained from OGTT data

AU - Gjesing, Anette Marianne Prior

AU - Ribel-Madsen, Rasmus

AU - Harder, Marie Neergaard

AU - Eiberg, Hans

AU - Grarup, Niels

AU - Jørgensen, Torben

AU - Ekstrøm, Claus T

AU - Pedersen, Oluf

AU - Hansen, Torben

PY - 2015/5

Y1 - 2015/5

N2 - AIMS/HYPOTHESIS: We examined the extent to which surrogate measures of insulin release have shared genetic causes.METHODS: Genetic 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.RESULTS: We 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/INTERPRETATION: The 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.

AB - AIMS/HYPOTHESIS: We examined the extent to which surrogate measures of insulin release have shared genetic causes.METHODS: Genetic 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.RESULTS: We 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/INTERPRETATION: The 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.

U2 - 10.1007/s00125-015-3516-9

DO - 10.1007/s00125-015-3516-9

M3 - Journal article

C2 - 25660259

VL - 58

SP - 1006

EP - 1012

JO - Diabetologia

JF - Diabetologia

SN - 0012-186X

IS - 5

ER -

ID: 134748111