Gene-Diet Interactions in Type 2 Diabetes

被引:1
作者
Cornelis M.C. [1 ,2 ]
机构
[1] Department of Nutrition, Harvard School of Public Health, Boston, 02215, MA
[2] Channing Division of Network Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA
关键词
Carbohydrate; Case-control; Clinical trial; Diet; Epidemiology; Fiber; Gene; Genetic risk score; Genome-wide association; Genome-wide environment interaction; Genotype; Glucose homeostasis; Interaction; Mediterranean diet; Modification; Nutrigenetics; Nutrigenomics; Nutrition; Personalized nutrition; Population; Risk stratification; Saturated fat; Type; 2; diabetes; Western diet;
D O I
10.1007/s13668-014-0095-1
中图分类号
学科分类号
摘要
Type 2 diabetes (T2D) is thought to arise from an interaction between susceptibility genes and a diabetogenic environment. This review summarizes progress pertaining specifically to gene-diet interactions. Recent efforts have been population-based and have focused on established genetic and dietary risk factors for T2D. TCF7L2 × carbohydrate-quality and IRS1 × macronutrient-composition interactions are promising factors, but most studies of gene-diet interactions are conflicting or need follow-up. T2D genetic risk scores are powerful predictors of developing T2D, but whether they can be combined with dietary risk factors merits further study. Lack of statistical power, imprecise diet measures, and conceptual issues surrounding replication all challenge our efforts to characterize interactions. Collaborations are needed for optimal study designs in both hypothesis-testing and hypothesis-generating contexts. Continued investment in studies of gene-diet interactions may lead to novel mechanistic insights into T2D, opportunities for risk stratification, and ultimately to personalized nutrition to prevent the disease. © 2014, Springer Science+Business Media New York.
引用
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页码:302 / 323
页数:21
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  • [1] Hogan P., Dall T., Nikolov P., Economic costs of diabetes in the US in 2002, Diabetes C, 26, 3, pp. 917-932, (2003)
  • [2] International Diabetes Federation. IDF Diabetes Atlas, 6th edn. Brussels, Belg
  • [3] DeFronzo R.A., Pathogenesis of type 2 diabetes: metabolic and molecular implications for identifying diabetes genes, Diabetes , 5, 3, pp. 177-269, (1997)
  • [4] Permutt M.A., Wasson J., Cox N., Genetic epidemiology of diabetes, J Clin Inv, 115, 6, pp. 1431-1439, (2005)
  • [5] Poulsen P., Kyvik K.O., Vaag A., Beck-Nielsen H., Heritability of type II (non-insulin-dependent) diabetes mellitus and abnormal glucose tolerance–a population-based twin study, Diabetolo, 42, 2, pp. 139-145, (1999)
  • [6] Kaprio J., Tuomilehto J., Koskenvuo M., Et al., Concordance for type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes mellitus in a population-based cohort of twins in Finland, Diabetolo, 35, 11, pp. 1060-1067, (1992)
  • [7] Morris A.P., Voight B.F., Teslovich T.M., Et al., Large-scale association analysis provides insights into the genetic architecture and pathophysiology of type 2 diabetes, Nat Ge, 44, 9, pp. 981-990, (2012)
  • [8] Dupuis J., Langenberg C., Prokopenko I., Et al., New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk, Nat Ge, 42, 2, pp. 105-116, (2010)
  • [9] Strawbridge R.J., Dupuis J., Prokopenko I., Et al., Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes, Diabe, 60, 10, pp. 2624-2634, (2011)
  • [10] Florez J.C., Newly identified loci highlight beta cell dysfunction as a key cause of type 2 diabetes: where are the insulin resistance genes?, Diabetolo, 51, 7, pp. 1100-1110, (2008)