| Budget Amount *help |
¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Research Abstract |
This study is a part of "The Hokkaido Study on Environment and Children's Health" as a prospective birth cohort. In this study, our objective is to evaluate the epidemiological effect of maternal PFCs exposure and peroxisome proliferator activating-receptors pathway polymorphisms on maternal lipid profile, birth outcome (birth weight, birth size), and children’s growth until school age.Prenatal levels of PFC compounds including PFOA and PFOS are available in maternal serum samples (n=514) between 2002 and 2005. Concentration of these chemicals were measured by liquid chromatography tandem mass spectrometry (LC-MS/MS). Primers for SNPs determination of following gens were purchased: PPARs (α, β, and γ), Leptin, LXR, HNF4α, and CAR. 400 μl of maternal whole blood samples which are collected immediately after delivery were subjected to the genomic DNA extraction. Using EP1 system (Fluidigm), I am examining SNP genotyping by end-point reading after PCR method. This process will be finished until 2014, September. After finishing genetic analysis, we assess the effect of prenatal PFCs exposure in underlying genetic background (SNPs in PPAR and PPAR-related pathways) on maternal TG and fatty acids during pregnancy. It may result in low birth size, and birth weight. Also, we are going to observe longitudinal effects of these chemical and genetic factors on child’s growth until school age. Therefore, we can identify of high risk groups classified by genetic susceptibility to PFCs exposure as a novel national pattern of environment-genetic interaction in Japanese population.
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