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Genetic variant in the IGF2BP2 gene may interact with fetal malnutrition to affect glucose metabolism.
Diabetes 2009; 58(6):1440-4D

Abstract

OBJECTIVE

Fetal malnutrition may predispose to type 2 diabetes through gene programming and developmental changes. Previous studies showed that these effects may be modulated by genetic variation. Genome-wide association studies discovered and replicated a number of type 2 diabetes-associated genes. We investigated the effects of such well-studied polymorphisms and their interactions with fetal malnutrition on type 2 diabetes risk and related phenotypes in the Dutch Famine Birth Cohort.

RESEARCH DESIGN AND METHODS

The rs7754840 (CDKAL1), rs10811661 (CDKN2AB), rs1111875 (HHEX), rs4402960 (IGF2BP2), rs5219 (KCNJ11), rs13266634 (SLC30A8), and rs7903146 (TCF7L2) polymorphisms were genotyped in 772 participants of the Dutch Famine Birth Cohort Study (n = 328 exposed, n = 444 unexposed). Logistic and linear regression models served to analyze their interactions with prenatal exposure to famine on type 2 diabetes, impaired glucose tolerance (IGT), and area under the curves (AUCs) for glucose and insulin during oral glucose tolerance testing (OGTT).

RESULTS

In the total population, the TCF7L2 and IGF2BP2 variants most strongly associated with increased risk for type 2 diabetes/IGT and increased AUC for glucose, while the CDKAL1 polymorphism associated with decreased AUC for insulin. The IGF2BP2 polymorphism showed an interaction with prenatal exposure to famine on AUC for glucose (beta = -9.2 [95% CI -16.2 to -2.1], P = 0.009).

CONCLUSIONS

The IGF2BP2 variant showed a nominal interaction with exposure to famine in utero, decreasing OGTT AUCs for glucose. This may provide a clue that modulation of the consequences of fetal environment depends on an individual's genetic background.

Authors+Show Affiliations

Department of Internal Medicine, Erasmus University Medical Center, Rotterdam, the Netherlands.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19258437

Citation

van Hoek, Mandy, et al. "Genetic Variant in the IGF2BP2 Gene May Interact With Fetal Malnutrition to Affect Glucose Metabolism." Diabetes, vol. 58, no. 6, 2009, pp. 1440-4.
van Hoek M, Langendonk JG, de Rooij SR, et al. Genetic variant in the IGF2BP2 gene may interact with fetal malnutrition to affect glucose metabolism. Diabetes. 2009;58(6):1440-4.
van Hoek, M., Langendonk, J. G., de Rooij, S. R., Sijbrands, E. J., & Roseboom, T. J. (2009). Genetic variant in the IGF2BP2 gene may interact with fetal malnutrition to affect glucose metabolism. Diabetes, 58(6), pp. 1440-4. doi:10.2337/db08-1173.
van Hoek M, et al. Genetic Variant in the IGF2BP2 Gene May Interact With Fetal Malnutrition to Affect Glucose Metabolism. Diabetes. 2009;58(6):1440-4. PubMed PMID: 19258437.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genetic variant in the IGF2BP2 gene may interact with fetal malnutrition to affect glucose metabolism. AU - van Hoek,Mandy, AU - Langendonk,Janneke G, AU - de Rooij,Susanne R, AU - Sijbrands,Eric J G, AU - Roseboom,Tessa J, Y1 - 2009/03/03/ PY - 2009/3/5/entrez PY - 2009/3/5/pubmed PY - 2009/7/18/medline SP - 1440 EP - 4 JF - Diabetes JO - Diabetes VL - 58 IS - 6 N2 - OBJECTIVE: Fetal malnutrition may predispose to type 2 diabetes through gene programming and developmental changes. Previous studies showed that these effects may be modulated by genetic variation. Genome-wide association studies discovered and replicated a number of type 2 diabetes-associated genes. We investigated the effects of such well-studied polymorphisms and their interactions with fetal malnutrition on type 2 diabetes risk and related phenotypes in the Dutch Famine Birth Cohort. RESEARCH DESIGN AND METHODS: The rs7754840 (CDKAL1), rs10811661 (CDKN2AB), rs1111875 (HHEX), rs4402960 (IGF2BP2), rs5219 (KCNJ11), rs13266634 (SLC30A8), and rs7903146 (TCF7L2) polymorphisms were genotyped in 772 participants of the Dutch Famine Birth Cohort Study (n = 328 exposed, n = 444 unexposed). Logistic and linear regression models served to analyze their interactions with prenatal exposure to famine on type 2 diabetes, impaired glucose tolerance (IGT), and area under the curves (AUCs) for glucose and insulin during oral glucose tolerance testing (OGTT). RESULTS: In the total population, the TCF7L2 and IGF2BP2 variants most strongly associated with increased risk for type 2 diabetes/IGT and increased AUC for glucose, while the CDKAL1 polymorphism associated with decreased AUC for insulin. The IGF2BP2 polymorphism showed an interaction with prenatal exposure to famine on AUC for glucose (beta = -9.2 [95% CI -16.2 to -2.1], P = 0.009). CONCLUSIONS: The IGF2BP2 variant showed a nominal interaction with exposure to famine in utero, decreasing OGTT AUCs for glucose. This may provide a clue that modulation of the consequences of fetal environment depends on an individual's genetic background. SN - 1939-327X UR - https://www.unboundmedicine.com/medline/citation/19258437/Genetic_variant_in_the_IGF2BP2_gene_may_interact_with_fetal_malnutrition_to_affect_glucose_metabolism_ L2 - http://diabetes.diabetesjournals.org/cgi/pmidlookup?view=long&pmid=19258437 DB - PRIME DP - Unbound Medicine ER -