Variations in Bitter-Taste Receptor Genes, Dietary Intake, and Colorectal Adenoma Risk

Abstract

Genetic variants in bitter-taste receptor genes have been hypothesized to negatively impact health outcomes and/or influence dietary intake and, consequently, could increase the risk of colorectal neoplasia. Using a case-control study of 914 colorectal adenoma cases/1188 controls, we explored associations among colorectal adenoma risk, dietary intake, and genetic variation in 3 bitter-taste receptor genes: TAS2R38 (rs713598, rs1726866, rs10246939), TAS2R16 (rs846672), and TAS2R50 (rs1376251). Analysis of covariance was conducted to detect trends in dietary intake across TAS2R genotypes/haplotypes. Odds ratios and 95% confidence intervals were estimated by logistic regression to test gene-adenoma risk associations. No significant associations were observed between the TAS2R38 PAV/PAV diplotype or the TAS2R16 (rs846672) polymorphism with the selected diet variables. We observed weak inverse associations between the TAS2R50 (rs1376251) C allele and dietary fiber and vegetable intake (Ps < 0.015). Odds ratios for adenoma risk were not significantly different from the null. Our findings do not support a link between these TAS2R genotypes/haplotypes and dietary intake that could impact colorectal adenoma risk. However, given the paucity of data, we cannot dismiss the possibility that these genes may influence colorectal adenoma risk in other ways, such as through impaired gastrointestinal function, particularly in subgroups of the population.

ACKNOWLEDGMENTS

This research was funded in part by the National Institutes of Health, National Cancer Institute (R01CA60987, CA72520). Susan M. Schembre was supported by postdoctoral fellowships on National Cancer Institute training grants at the University of Hawaii Cancer Center (R25CA90956) and the University of Southern California (T32CA009492) during the preparation of this manuscript. The authors thank Jean Sato and Barbara Saltzman for coordinating the data collection, Maj Earle and Anne Tome for data management, and Annette Lum-Jones for performing the laboratory assays. We also thank the Hawaii Tumor Registry (National Cancer Institute contract N01PC35137) for assistance in CRC case identification.