期刊
JOURNAL OF NUTRITION
卷 141, 期 2, 页码 177-181出版社
AMER SOC NUTRITION-ASN
DOI: 10.3945/jn.110.124206
关键词
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资金
- Federal Ministry of Science, Germany [01 EA 9401]
- European Union [SOC 95201408 05E02, SOC 98200769 05F02]
- German Cancer Aid [70-2488-Ha I]
- German Federal Ministry of Education and Research [AZ 0313437B/D]
Multiple genetic and environmental factors underlie the etiology of type 2 diabetes. To evaluate the influence of the relationship between dietary fat intake and single nucleotide polymorphisms (SNPs) in genes involved in fat assimilation on disease susceptibility, a 2-step approach using an exploratory case-control study (n = 192/384) and an independent, confirmatory case-cohort study (n = 614/2248) taken from the same prospective study population (European Prospective Investigation into Cancer and Nutrition-Potsdam) was used. Sixty-three SNPs in 32 genes were initially analyzed. Total intake of fat and fatty acid intake were calculated from validated baseline FFQ. The SNP x nutrient interaction was tested in multivariate adjusted regression models. The initial screening step revealed evidence that, for 4 SNPs (CAV2 rs2270188, DBI rs2084202, PPARG rs1801282, and SREBF1 rs2297508), disease susceptibility might depend on the amount and quality of fat intake. The insulin receptor regulator CAV2 rs2270188 G > T SNP was found to interact with dietary fat in the confirmatory case-cohort study. Using pooled data, homozygous individuals of the rare T-allele showed a 100% greater risk of type 2 diabetes if daily fat intake was increased from 30 to 40 % energy. An increase in dietary SFA from 10 to 20 % energy predicted an similar to 200% greater risk of type 2 diabetes. We found preliminary evidence that CAV2 rs2270188 interacts with dietary fat to affect risk of type 2 diabetes. J. Nutr. 141: 177-181, 2011.
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