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Interaction between genes and macronutrient intake on the risk of developing type 2 diabetes : Systematic review and findings from European Prospective Investigation into Cancer (EPIC)-InterAct

Li, Sherly X.; Imamura, Fumiaki; Ye, Zheng; Schulze, Matthias B; Zheng, Jusheng; Ardanaz, Eva; Arriola, Larraitz; Boeing, Heiner; Dow, Courtney and Fagherazzi, Guy, et al. (2017) In American Journal of Clinical Nutrition 106(1). p.263-275
Abstract

Background: Gene-diet interactions have been reported to contribute to the development of type 2 diabetes (T2D). However, to our knowledge, few examples have been consistently replicated to date. Objective: We aimed to identify existing evidence for genemacronutrient interactions and T2D and to examine the reported interactions in a large-scale study. Design: We systematically reviewed studies reporting genemacronutrient interactions and T2D. We searched the MEDLINE, Human Genome Epidemiology Network, and WHO International Clinical Trials Registry Platform electronic databases to identify studies published up to October 2015. Eligibility criteria included assessment of macronutrient quantity (e.g., total carbohydrate) or indicators of... (More)

Background: Gene-diet interactions have been reported to contribute to the development of type 2 diabetes (T2D). However, to our knowledge, few examples have been consistently replicated to date. Objective: We aimed to identify existing evidence for genemacronutrient interactions and T2D and to examine the reported interactions in a large-scale study. Design: We systematically reviewed studies reporting genemacronutrient interactions and T2D. We searched the MEDLINE, Human Genome Epidemiology Network, and WHO International Clinical Trials Registry Platform electronic databases to identify studies published up to October 2015. Eligibility criteria included assessment of macronutrient quantity (e.g., total carbohydrate) or indicators of quality (e.g., dietary fiber) by use of self-report or objective biomarkers of intake. Interactions identified in the review were subsequently examined in the EPIC (European Prospective Investigation into Cancer)-InterAct case-cohort study (n = 21,148, with 9403 T2D cases; 8 European countries). Prentice-weighted Cox regression was used to estimate countryspecific HRs, 95% CIs, and P-interaction values, which were then pooled by random-effects meta-analysis. A primary model was fitted by using the same covariates as reported in the published studies, and a second model adjusted for additional covariates and estimated the effects of isocaloric macronutrient substitution. Results: Thirteen observational studies met the eligibility criteria (n < 1700 cases). Eight unique interactions were reported to be significant between macronutrients [carbohydrate, fat, saturated fat, dietary fiber, and glycemic load derived from self-report of dietary intake and circulating n-3 (v-3) polyunsaturated fatty acids] and genetic variants in or near transcription factor 7-like 2 (TCF7L2), gastric inhibitory polypeptide receptor (GIPR), caveolin 2 (CAV2), and peptidase D (PEPD) (P-interaction < 0.05). We found no evidence of interaction when we tried to replicate previously reported interactions. In addition, no interactions were detected in models with additional covariates. Conclusions: Eight gene-macronutrient interactions were identified for the risk of T2D from the literature. These interactions were not replicated in the EPIC-InterAct study, which mirrored the analyses undertaken in the original reports. Our findings highlight the importance of independent replication of reported interactions. Am J Clin Nutr 2017;106:263-75.

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keywords
Diabetes, Diet, Effect modification, Gene, Interaction, Macronutrient, Replication, Systematic review
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American Journal of Clinical Nutrition
volume
106
issue
1
pages
13 pages
publisher
American Society for Clinical Nutrition
external identifiers
  • scopus:85021813265
  • wos:000404593900033
ISSN
0002-9165
DOI
10.3945/ajcn.116.150094
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English
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yes
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755e4996-b952-444f-93a5-777faa86bc80
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2017-08-08 16:41:07
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2017-09-18 11:41:10
@article{755e4996-b952-444f-93a5-777faa86bc80,
  abstract     = {<p>Background: Gene-diet interactions have been reported to contribute to the development of type 2 diabetes (T2D). However, to our knowledge, few examples have been consistently replicated to date. Objective: We aimed to identify existing evidence for genemacronutrient interactions and T2D and to examine the reported interactions in a large-scale study. Design: We systematically reviewed studies reporting genemacronutrient interactions and T2D. We searched the MEDLINE, Human Genome Epidemiology Network, and WHO International Clinical Trials Registry Platform electronic databases to identify studies published up to October 2015. Eligibility criteria included assessment of macronutrient quantity (e.g., total carbohydrate) or indicators of quality (e.g., dietary fiber) by use of self-report or objective biomarkers of intake. Interactions identified in the review were subsequently examined in the EPIC (European Prospective Investigation into Cancer)-InterAct case-cohort study (n = 21,148, with 9403 T2D cases; 8 European countries). Prentice-weighted Cox regression was used to estimate countryspecific HRs, 95% CIs, and P-interaction values, which were then pooled by random-effects meta-analysis. A primary model was fitted by using the same covariates as reported in the published studies, and a second model adjusted for additional covariates and estimated the effects of isocaloric macronutrient substitution. Results: Thirteen observational studies met the eligibility criteria (n &lt; 1700 cases). Eight unique interactions were reported to be significant between macronutrients [carbohydrate, fat, saturated fat, dietary fiber, and glycemic load derived from self-report of dietary intake and circulating n-3 (v-3) polyunsaturated fatty acids] and genetic variants in or near transcription factor 7-like 2 (TCF7L2), gastric inhibitory polypeptide receptor (GIPR), caveolin 2 (CAV2), and peptidase D (PEPD) (P-interaction &lt; 0.05). We found no evidence of interaction when we tried to replicate previously reported interactions. In addition, no interactions were detected in models with additional covariates. Conclusions: Eight gene-macronutrient interactions were identified for the risk of T2D from the literature. These interactions were not replicated in the EPIC-InterAct study, which mirrored the analyses undertaken in the original reports. Our findings highlight the importance of independent replication of reported interactions. Am J Clin Nutr 2017;106:263-75.</p>},
  author       = {Li, Sherly X. and Imamura, Fumiaki and Ye, Zheng and Schulze, Matthias B and Zheng, Jusheng and Ardanaz, Eva and Arriola, Larraitz and Boeing, Heiner and Dow, Courtney and Fagherazzi, Guy and Franks, Paul W. and Agudo, Antonio and Grioni, Sara and Kaaks, Rudolf and Katzke, Verena A. and Key, Timothy J and Khaw, Kay Tee and Mancini, Francesca Romana and Navarro, Carmen and Nilsson, Peter M. and Onland-Moret, N. Charlotte and Overvad, Kim and Palli, Domenico and Panico, Salvatore and Quirós, J Ramón and Rolandsson, Olov and Sacerdote, Carlotta and Sánchez, María-José and Slimani, Nadia and Sluijs, Ivonne and Spijkerman, Annemieke M. W. and Tjonneland, Anne and Tumino, Rosario and Sharp, Stephen J. and Riboli, Elio and Langenberg, Claudia and Scott, Robert A. and Forouhi, Nita G. and Wareham, Nicholas J},
  issn         = {0002-9165},
  keyword      = {Diabetes,Diet,Effect modification,Gene,Interaction,Macronutrient,Replication,Systematic review},
  language     = {eng},
  month        = {07},
  number       = {1},
  pages        = {263--275},
  publisher    = {American Society for Clinical Nutrition},
  series       = {American Journal of Clinical Nutrition},
  title        = {Interaction between genes and macronutrient intake on the risk of developing type 2 diabetes : Systematic review and findings from European Prospective Investigation into Cancer (EPIC)-InterAct},
  url          = {http://dx.doi.org/10.3945/ajcn.116.150094},
  volume       = {106},
  year         = {2017},
}