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ARS Home » Plains Area » Grand Forks, North Dakota » Grand Forks Human Nutrition Research Center » Dietary Prevention of Obesity-related Disease Research » Research » Publications at this Location » Publication #259871
Title: Differential responses to selenomethioinine supplementation by sex and genotype in healthy adults

Author
item Combs, Gerald
item Jackson, Matthew
item Watts, Jennifer
item JOHNSON, LUANN - University Of North Dakota
item Zeng, Huawei
item Idso, Joseph
item SCHOMBURG, LUTZ - Charite' University Hospital Berlin
item HOEG, ANTONIA - Charite' University Hospital Berlin
item HOEFIG, CAROLIN - Charite' University Hospital Berlin
item CHIANG, EMILY - Gerald P Murphy Cancer Foundation
item WATERS, DAVID - Gerald P Murphy Cancer Foundation
item TSUJI, PETRA - National Cancer Institute (NCI, NIH)
item DAVIS, CINDY - National Cancer Institute (NCI, NIH)
item MILNER, JOHN - National Cancer Institute (NCI, NIH)

Submitted to: British Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/21/2011
Publication Date: 5/12/2012
Citation: Combs, G.F., Jackson, M.I., Watts, J.J., Johnson, L.K., Zeng, H., Idso, J.P., Schomburg, L., Hoeg, A., Hoefig, C.S., Chiang, E.C., Waters, D.J., Tsuji, P.A., Davis, C.D., Milner, J.A. 2012. Differential responses to selenomethioinine supplementation by sex and genotype in healthy adults. British Journal of Nutrition. 107:1514-1525.

Interpretive Summary: Because selenium (Se) supplementation has been shown to reduce cancer risk in subjects with initial plasma Se concentrations <106 ng/ml, it would be useful to know the Se intake required to achieve such a threshold. We conducted a randomized, double-blind, intervention trial to determine the responses of multiple biomarkers of Se status in 216 healthy adults during a year-long intervention with selenomethionine (SeMet). We measured the responses of several biomarkers of Se status relative to genotype of four selenoproteins, dietary Se intake and parameters of single-carbon metabolism. We found supplemental SeMet not to affect plasma activities of two Se-dependent proteins, glutathione peroxidase and selenoprotein P, but produced significant, dose-dependent increases in the Se contents of plasma, urine and buccal cells that plateaued by 9-12 mos and were linearly related to effective Se dose (µg/day/kg0.75). The increase in urinary Se excretion was greater for women than men, and for individuals of the GPX1 679 T/T genotype than for those of the GPX1 679 C/C genotype. Our results show that, for non-deficient adults, the Se intake (as SeMet) required to support plasma Se concentration at a target level (Sepl-target) is: Sein = (Sepl-target - Sepl)/18.2 ng d kg0.75 ml-1ug-1.

Technical Abstract: Background: Selenium (Se) supplementation may reduce cancer risk in subjects with initial plasma Se concentrations <106 ng/ml. It would be useful to know the Se intake required to achieve such a threshold. Objective: Characterize the responses of multiple biomarkers of Se status in healthy adults during a year-long intervention with selenomethionine (SeMet). Design: A total of 261 men and women were randomized to four doses of Se (0, 50, 100 or 200 µg/day as L-SeMet) for 12 months. Responses of several biomarkers of Se status (plasma Se, plasma seleoprotein P [SEPP1], plasma glutathione peroxidase activity [GPX3], buccal cell Se, urinary Se) were determined relative to genotype of four selenoproteins (GPX1, GPX3, SEPP1, selenoprotein 15 [SEP15]), dietary Se intake and parameters of single-carbon metabolism. Results: Supplemental SeMet did not affect GPX3 activity or SEPP1 concentration, but produced significant, dose-dependent increases in the Se contents of plasma, urine and buccal cells that plateaued by 9-12 mos and were linearly related to effective Se dose (µg/day/kg0.75). The increase in urinary Se excretion was greater for women than men, and for individuals of the GPX1 679 T/T genotype than for those of the GPX1 679 C/C genotype. Conclusions: The most responsive biomarkers of Se status were those related to body Se pools: plasma, buccal cell, urinary Se concentrations. The change in plasma Se resulted from increases in its non-specific component. For non-deficient adults, the Se intake (as SeMet) required to support plasma Se concentration at a target level (Sepl-target) is: Sein= (Sepl-target – Sepl)/18.2 ng d kg0.75 ml-1ug-1.