Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes

Sara Krogh Hansen; Eva-Maria D Nielsen; Jakob Ek; Gitte Andersen; Charlotte Glümer; Bendix Carstensen; Peter Mouritzen; Thomas Drivsholm; Knut Borch-Johnsen; Torben Jørgensen; Torben Hansen; Oluf Pedersen

doi:10.1210/jc.2004-1942

Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes

Sara Krogh Hansen, Eva-Maria D Nielsen, Jakob Ek, Gitte Andersen, Charlotte Glümer, Bendix Carstensen, Peter Mouritzen, Thomas Drivsholm, Knut Borch-Johnsen, Torben Jørgensen, Torben Hansen, Oluf Pedersen

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Abstract

The separate and combined effects of the PPARG Pro(12)Ala polymorphism and the KCNJ11 Glu(23)Lys polymorphisms on risk of type 2 diabetes were investigated in relatively large-scale, case-control studies. Separate effects of the variants were examined among 1187/1461 type 2 diabetic patients and 4791/4986 middle-aged, glucose-tolerant subjects. The combined analysis involved 1164 type 2 diabetic patients and 4733 middle-aged, glucose-tolerant subjects. In the separate analyses, the K allele of the KCNJ11 Glu(23)Lys associated with type 2 diabetes (odds ratio, 1.19; P = 0.0002), whereas the PPARG Pro(12)Ala showed no significant association with type 2 diabetes. The combined analysis indicated that the two polymorphisms acted in an additive manner to increase the risk of type 2 diabetes, and we found no evidence for a synergistic interaction between them. Analysis of a model with equal additive effects of the two variants showed that the odds ratio for type 2 diabetes increased with 1.14/risk allele (P = 0.003). Together, the two polymorphisms conferred a population-attributable risk for type 2 diabetes of 28%. In conclusion, our results showed no evidence of a synergistic interaction between the KCNJ11 Glu(23)Lys and PPARG Pro(12)Ala polymorphisms, but indicated that they may act in an additive manner to increase the risk of type 2 diabetes.

Originalsprog	Engelsk
Tidsskrift	Journal of Clinical Endocrinology and Metabolism
Vol/bind	90
Udgave nummer	6
Sider (fra-til)	3629-37
Antal sider	9
ISSN	0021-972X
DOI	https://doi.org/10.1210/jc.2004-1942
Status	Udgivet - 1 jun. 2005

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Hansen, S. K., Nielsen, E-M. D., Ek, J., Andersen, G., Glümer, C., Carstensen, B., Mouritzen, P., Drivsholm, T., Borch-Johnsen, K., Jørgensen, T., Hansen, T., & Pedersen, O. (2005). Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes. Journal of Clinical Endocrinology and Metabolism, 90(6), 3629-37. https://doi.org/10.1210/jc.2004-1942

Hansen, SK, Nielsen, E-MD, Ek, J, Andersen, G, Glümer, C, Carstensen, B, Mouritzen, P, Drivsholm, T, Borch-Johnsen, K, Jørgensen, T, Hansen, T & Pedersen, O 2005, 'Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes', Journal of Clinical Endocrinology and Metabolism, bind 90, nr. 6, s. 3629-37. https://doi.org/10.1210/jc.2004-1942

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title = "Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes",

abstract = "The separate and combined effects of the PPARG Pro(12)Ala polymorphism and the KCNJ11 Glu(23)Lys polymorphisms on risk of type 2 diabetes were investigated in relatively large-scale, case-control studies. Separate effects of the variants were examined among 1187/1461 type 2 diabetic patients and 4791/4986 middle-aged, glucose-tolerant subjects. The combined analysis involved 1164 type 2 diabetic patients and 4733 middle-aged, glucose-tolerant subjects. In the separate analyses, the K allele of the KCNJ11 Glu(23)Lys associated with type 2 diabetes (odds ratio, 1.19; P = 0.0002), whereas the PPARG Pro(12)Ala showed no significant association with type 2 diabetes. The combined analysis indicated that the two polymorphisms acted in an additive manner to increase the risk of type 2 diabetes, and we found no evidence for a synergistic interaction between them. Analysis of a model with equal additive effects of the two variants showed that the odds ratio for type 2 diabetes increased with 1.14/risk allele (P = 0.003). Together, the two polymorphisms conferred a population-attributable risk for type 2 diabetes of 28%. In conclusion, our results showed no evidence of a synergistic interaction between the KCNJ11 Glu(23)Lys and PPARG Pro(12)Ala polymorphisms, but indicated that they may act in an additive manner to increase the risk of type 2 diabetes.",

author = "Hansen, {Sara Krogh} and Nielsen, {Eva-Maria D} and Jakob Ek and Gitte Andersen and Charlotte Gl{\"u}mer and Bendix Carstensen and Peter Mouritzen and Thomas Drivsholm and Knut Borch-Johnsen and Torben J{\o}rgensen and Torben Hansen and Oluf Pedersen",

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AU - Hansen, Sara Krogh

AU - Nielsen, Eva-Maria D

AU - Ek, Jakob

AU - Andersen, Gitte

AU - Glümer, Charlotte

AU - Carstensen, Bendix

AU - Mouritzen, Peter

AU - Drivsholm, Thomas

AU - Borch-Johnsen, Knut

AU - Jørgensen, Torben

AU - Hansen, Torben

AU - Pedersen, Oluf

PY - 2005/6/1

Y1 - 2005/6/1

N2 - The separate and combined effects of the PPARG Pro(12)Ala polymorphism and the KCNJ11 Glu(23)Lys polymorphisms on risk of type 2 diabetes were investigated in relatively large-scale, case-control studies. Separate effects of the variants were examined among 1187/1461 type 2 diabetic patients and 4791/4986 middle-aged, glucose-tolerant subjects. The combined analysis involved 1164 type 2 diabetic patients and 4733 middle-aged, glucose-tolerant subjects. In the separate analyses, the K allele of the KCNJ11 Glu(23)Lys associated with type 2 diabetes (odds ratio, 1.19; P = 0.0002), whereas the PPARG Pro(12)Ala showed no significant association with type 2 diabetes. The combined analysis indicated that the two polymorphisms acted in an additive manner to increase the risk of type 2 diabetes, and we found no evidence for a synergistic interaction between them. Analysis of a model with equal additive effects of the two variants showed that the odds ratio for type 2 diabetes increased with 1.14/risk allele (P = 0.003). Together, the two polymorphisms conferred a population-attributable risk for type 2 diabetes of 28%. In conclusion, our results showed no evidence of a synergistic interaction between the KCNJ11 Glu(23)Lys and PPARG Pro(12)Ala polymorphisms, but indicated that they may act in an additive manner to increase the risk of type 2 diabetes.

AB - The separate and combined effects of the PPARG Pro(12)Ala polymorphism and the KCNJ11 Glu(23)Lys polymorphisms on risk of type 2 diabetes were investigated in relatively large-scale, case-control studies. Separate effects of the variants were examined among 1187/1461 type 2 diabetic patients and 4791/4986 middle-aged, glucose-tolerant subjects. The combined analysis involved 1164 type 2 diabetic patients and 4733 middle-aged, glucose-tolerant subjects. In the separate analyses, the K allele of the KCNJ11 Glu(23)Lys associated with type 2 diabetes (odds ratio, 1.19; P = 0.0002), whereas the PPARG Pro(12)Ala showed no significant association with type 2 diabetes. The combined analysis indicated that the two polymorphisms acted in an additive manner to increase the risk of type 2 diabetes, and we found no evidence for a synergistic interaction between them. Analysis of a model with equal additive effects of the two variants showed that the odds ratio for type 2 diabetes increased with 1.14/risk allele (P = 0.003). Together, the two polymorphisms conferred a population-attributable risk for type 2 diabetes of 28%. In conclusion, our results showed no evidence of a synergistic interaction between the KCNJ11 Glu(23)Lys and PPARG Pro(12)Ala polymorphisms, but indicated that they may act in an additive manner to increase the risk of type 2 diabetes.

U2 - 10.1210/jc.2004-1942

DO - 10.1210/jc.2004-1942

M3 - Journal article

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JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

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ER -

Analysis of separate and combined effects of common variation in KCNJ11 and PPARG on risk of type 2 diabetes

Abstract

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