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Interactions of Peroxisome Proliferator–Activated Receptor and Diet in Etiology of Colorectal Cancer

¹ Health Research Center, Departments of Family and Preventive Medicine and ² Pathology, University of Utah School of Medicine, Salt Lake City, Utah; ³ Division of Research, Kaiser Permanente Oakland, California; and ⁴ Fred Hutchinson Cancer Research Center, Seattle, Washington

Requests for reprints: Maureen A. Murtaugh, Health Research Center, Department of Family and Preventive Medicine, University of Utah, Suite A, 375 Chipeta Way, Salt Lake City, UT 84101. Phone: 801-585-9216; Fax: 801-581-3623. E-mail: mmurtaugh{at}hrc.utah.edu

The peroxisome proliferator–activated receptor (PPAR) is one of a group of ligand-activated nuclear receptors responsible for regulation of glucose, lipid homeostasis, cell differentiation, and apoptosis. The 12 proline-to-alanine (Pro12Ala) substitution polymorphism in PPAR produces proteins with lower activity. Variation in PPAR expression in the bowel and the role of dietary fatty acids as ligands for PPAR led investigation of whether the associations of diet with colon and rectal cancer risk were modified by PPAR genotype. Data (diet, lifestyle, and DNA) came from case-control studies of colon (1,577 cases and 1,971 controls) and rectal cancer (794 cases and 1,001 controls) conducted in Northern California, Utah, and the Twin City, Minnesota Metropolitan area (colon cancer study only). Unconditional logistic regression models were adjusted for age at selection, body mass index, physical activity, energy intake, dietary fiber, and calcium. We found no significant interactions between macronutrient (fat, protein, and carbohydrate) and colorectal cancer. High lutein intake [odds ratio (OR), 0.63; 95% confidence interval (95% CI), 0.44-0.89], low refined grain intake (OR, 0.70; 95% CI, 0.53-0.94), or a high prudent diet score (OR, 0.66; 95% CI, 0.49-0.89) and PA/AA PPAR genotype were associated with reduced colon cancer risk. Risk of rectal cancer was increased among those with the PA/AA PPAR genotype and a high mutagen index (OR, 1.63; 95% CI, 1.12, 2.36). Its unclear whether the alterations in risk in those with the less active phenotype for PPAR is related to activation of PPAR by nutrients or dietary patterns acting as ligands or direct influences of these nutrients on colon and rectal cancer processes that are important with lower PPAR activity.

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