Browsing by Author "Oppeneer, Sarah"
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Item Bisphenol A, Diet and Obesity: Exposure Measurement and the Relationship Between Diet and Bisphenol A(2014-01) Oppeneer, SarahDiet is considered the primary source of BPA exposure, due to the use of BPA in polycarbonate plastics and epoxy resins used in food packaging. Existing human research has major limitations and the cost of serum and urinary BPA assay remains a challenge in evaluating BPA exposure and chronic disease outcomes. Despite the fact that diet is a vehicle for BPA exposure, few studies have considered whether dietary composition alters the toxicokinetics of BPA. Epidemiological studies have also not addressed diet as a potential confounder or effect modifier even though diet is associated with both disease risk and BPA exposure. The Urinary Biomarkers of Dietary Intake (UB-Diet Study) was developed to evaluate the feasibility of using questions that target intake of known dietary sources of BPA to estimate BPA exposure. Predicted BPA exposure levels from the BPA exposure assessment module (BEAM) were compared to multiple spot urine samples. Food records were also collected on the days that urine samples were collected to further evaluate the relationship between diet and urinary BPA levels. Reported macronutrient and food group servings were compared to urinary BPA levels. The BEAM data was not able to accurately predict participants' urinary BPA levels. Recent canned food intake was associated with urinary BPA levels, but only explained approximately one-fifth of the variability in urinary BPA levels and several participants who reported consuming no canned foods had high urinary BPA levels. The study findings suggest that BPA levels may be positively associated with higher caloric and fiber intake, and intakes of vegetables, refined grains and red meats, and inversely associated with total fat intake. More research is needed to characterize sources of BPA exposure, to evaluate the role of diet in the toxicokinetics of BPA and to determine if chronic low level BPA exposure poses any health risk.Item Impact of FPGS and GGH SNPs on plasma folate and homocysteine levels in the Singapore Chinese health study.(2010-06) Oppeneer, SarahBackground: Folate has widespread importance to health due to its role in one-carbon metabolism. Folate status and genetic variants in the folate uptake and metabolism pathways have been assessed in relation to numerous disease processes, especially colon cancer and cardiovascular disease. The enzymes folylpolyglutamate synthase (FPGS) and gamma-glutamyl hydrolase (GGH) are essential for maintaining intracellular folate homeostasis. FPGS adds glutamyl groups to the folate molecule, which is essential for cellular retention of folate. The polyglutamted form of folate metabolites is the preferred substrate for many one-carbon metabolism enzymes. GGH removes glutamyl groups, which allows folate to leave the cell. Objective: The purpose of this study was to evaluate whether single nucleotide polymorphisms (SNPs) in the FPGS and GGH genes influence plasma folate and homocysteine levels. Methods: Study participants were a sub-cohort (n = 484) from the Singapore Chinese Health Study. SNPs were selected using a literature review, HapMap, and SNPPer. Multiple linear regression was used to evaluate the association between the SNPs and plasma folate and homocysteine levels. Results: Two FPGS (rs10106, rs1098774) and 9 GGH (rs1031552, rs11545076, rs1800909, rs3758149, rs3780126, rs3824333, rs4617146, rs11545078, rs719235) SNPs were included in the final analysis. None of the FPGS or GGH SNPs were associated with plasma folate levels. Similarly, none of the FPGS SNPs were associated with plasma homocysteine, but three GGH SNPs were associated with plasma homocysteine levels: rs11545076 (p = 0.02), rs1800909 (p = 0.03), and rs3758149 (p = 0.04). In all three, the homozygous variant alleles were associated with lower plasma homocysteine values. Conclusions: It appears that genetic variation in GGH may be influential in determining circulating homocysteine levels, and thus, may influence intracellular folate homeostasis rather than circulating folate levels. Since this is one of the first studies to assess these genetic variants in relation to plasma folate and homocysteine, further research is needed to explore these variants and to better characterize the role of genetic variation in intracellular folate homeostasis.