Differential responses to selenomethionine supplementation by sex and genotype in healthy adults

• Published in: British journal of nutrition 2012-05, Vol.107 (10), p.1514-1525
• Main Authors: Combs, Gerald F., Jackson, Matthew I., Watts, Jennifer C., Johnson, LuAnn K., Zeng, Huawei, Idso, Joseph, Schomburg, Lutz, Hoeg, Antonia, Hoefig, Carolin S., Chiang, Emily C., Waters, David J., Davis, Cindy D., Milner, John A.
• Format: Article
• Language: English
• Subjects: Adult; Aged; Biological and medical sciences; Biomarkers - metabolism; Carbon - metabolism; Dietary minerals; Dietary Supplements; Dose-Response Relationship, Drug; Feeding. Feeding behavior; Female; Fundamental and applied biological sciences. Psychology; Gender differences; Genotype; Genotype & phenotype; Glutathione Peroxidase - genetics; Glutathione Peroxidase - metabolism; Glutathione Peroxidase GPX1; Human and Clinical Nutrition; Humans; Male; Middle Aged; Mouth - cytology; Mouth - metabolism; Mouth Mucosa - cytology; Mouth Mucosa - metabolism; Nutrition research; Selenium - blood; Selenium - metabolism; Selenium - urine; Selenomethionine - pharmacokinetics; Selenoprotein P - metabolism; Selenoproteins - genetics; Selenoproteins - metabolism; Sex Factors; Vertebrates: anatomy and physiology, studies on body, several organs or systems
• ISSN: 0007-1145; 1475-2662
• DOI: 10.1017/S0007114511004715

A year-long intervention trial was conducted to characterise the responses of multiple biomarkers of Se status in healthy American adults to supplemental selenomethionine (SeMet) and to identify factors affecting those responses. A total of 261 men and women were randomised to four doses of Se (0, 50, 100 or 200 μg/d as l-SeMet) for 12 months. Responses of several biomarkers of Se status (plasma Se, serum selenoprotein 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), dietary Se intake and parameters of single-carbon metabolism. Results showed that 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, each of which plateaued by 9–12 months and was linearly related to effective Se dose (μg/d per 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. It is concluded that the most responsive Se-biomarkers in this non-deficient cohort were those related to body Se pools: plasma, buccal cell and urinary Se concentrations. Changes in plasma Se resulted from increases in its non-specific component and were affected by both sex and GPX1 genotype. In a cohort of relatively high Se status, the Se intake (as SeMet) required to support plasma Se concentration at a target level (Sepl-target) is: Se_{in} = [(Se_{pl - target} - Se_{pl})/(18.2\hairsp ng\,d\,kg^{0.75}/ml\,per\,\mu g)] .