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Selenium deficiency occurs in some patients with moderate-to-severe cirrhosis and can be corrected by administration of selenate but not selenomethionine: a randomized controlled trial.

Abstract

BACKGROUND

Selenomethionine, which is the principal dietary form of selenium, is metabolized by the liver to selenide, which is the form of the element required for the synthesis of selenoproteins. The liver synthesizes selenium-rich selenoprotein P (SEPP1) and secretes it into the plasma to supply extrahepatic tissues with selenium.

OBJECTIVES

We conducted a randomized controlled trial to determine whether cirrhosis is associated with functional selenium deficiency (the lack of selenium for the process of selenoprotein synthesis even though selenium intake is not limited) and, if it is, whether the deficiency is associated with impairment of selenomethionine metabolism.

DESIGN

Patients with Child-Pugh (C-P) classes A, B, and C (mild, moderate, and severe, respectively) cirrhosis were supplemented with a placebo or supranutritional amounts of selenium as selenate (200 or 400 μg/d) or as selenomethionine (200 μg/d) for 4 wk. Plasma SEPP1 concentration and glutathione peroxidase (GPX) activity, the latter due largely to the selenoprotein GPX3 secreted by the kidneys, were measured before and after supplementation.

RESULTS

GPX activity was increased more by both doses of selenate than by the placebo in C-P class B patients. The activity was not increased more by selenomethionine supplementation than by the placebo in C-P class B patients. Plasma selenium was increased more by 400 μg Se as selenate than by the placebo in C-P class C patients. Within the groups who responded to selenate, there was a considerable variation in responses.

CONCLUSION

These results indicate that severe cirrhosis causes mild functional selenium deficiency in some patients that is associated with impaired metabolism of selenomethionine. This trial was registered at clinicaltrials.gov as NCT00271245.

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  • Authors+Show Affiliations

    ,

    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and raymond.burk@vanderbilt.edu.

    ,

    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and.

    ,

    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and.

    ,

    Department of Biostatistics, Vanderbilt University School of Medicine, Nashville, TN.

    Division of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, and.

    Source

    MeSH

    Adult
    Biomarkers
    Deficiency Diseases
    Dietary Supplements
    Female
    Glutathione Peroxidase
    Humans
    Incidence
    Liver Cirrhosis
    Male
    Methionine
    Middle Aged
    Nutritional Status
    Pilot Projects
    Selenic Acid
    Selenium
    Selenomethionine
    Selenoprotein P
    Severity of Illness Index
    Tennessee

    Pub Type(s)

    Comparative Study
    Journal Article
    Randomized Controlled Trial
    Research Support, N.I.H., Extramural

    Language

    eng

    PubMed ID

    26468123

    Citation

    Burk, Raymond F., et al. "Selenium Deficiency Occurs in some Patients With Moderate-to-severe Cirrhosis and Can Be Corrected By Administration of Selenate but Not Selenomethionine: a Randomized Controlled Trial." The American Journal of Clinical Nutrition, vol. 102, no. 5, 2015, pp. 1126-33.
    Burk RF, Hill KE, Motley AK, et al. Selenium deficiency occurs in some patients with moderate-to-severe cirrhosis and can be corrected by administration of selenate but not selenomethionine: a randomized controlled trial. Am J Clin Nutr. 2015;102(5):1126-33.
    Burk, R. F., Hill, K. E., Motley, A. K., Byrne, D. W., & Norsworthy, B. K. (2015). Selenium deficiency occurs in some patients with moderate-to-severe cirrhosis and can be corrected by administration of selenate but not selenomethionine: a randomized controlled trial. The American Journal of Clinical Nutrition, 102(5), pp. 1126-33. doi:10.3945/ajcn.115.110932.
    Burk RF, et al. Selenium Deficiency Occurs in some Patients With Moderate-to-severe Cirrhosis and Can Be Corrected By Administration of Selenate but Not Selenomethionine: a Randomized Controlled Trial. Am J Clin Nutr. 2015;102(5):1126-33. PubMed PMID: 26468123.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Selenium deficiency occurs in some patients with moderate-to-severe cirrhosis and can be corrected by administration of selenate but not selenomethionine: a randomized controlled trial. AU - Burk,Raymond F, AU - Hill,Kristina E, AU - Motley,Amy K, AU - Byrne,Daniel W, AU - Norsworthy,Brooke K, Y1 - 2015/10/14/ PY - 2015/03/09/received PY - 2015/09/10/accepted PY - 2015/10/16/entrez PY - 2015/10/16/pubmed PY - 2016/2/9/medline KW - functional selenium deficiency KW - inorganic selenium metabolism KW - selenium biomarkers KW - selenium metabolism by the liver KW - selenium requirement SP - 1126 EP - 33 JF - The American journal of clinical nutrition JO - Am. J. Clin. Nutr. VL - 102 IS - 5 N2 - BACKGROUND: Selenomethionine, which is the principal dietary form of selenium, is metabolized by the liver to selenide, which is the form of the element required for the synthesis of selenoproteins. The liver synthesizes selenium-rich selenoprotein P (SEPP1) and secretes it into the plasma to supply extrahepatic tissues with selenium. OBJECTIVES: We conducted a randomized controlled trial to determine whether cirrhosis is associated with functional selenium deficiency (the lack of selenium for the process of selenoprotein synthesis even though selenium intake is not limited) and, if it is, whether the deficiency is associated with impairment of selenomethionine metabolism. DESIGN: Patients with Child-Pugh (C-P) classes A, B, and C (mild, moderate, and severe, respectively) cirrhosis were supplemented with a placebo or supranutritional amounts of selenium as selenate (200 or 400 μg/d) or as selenomethionine (200 μg/d) for 4 wk. Plasma SEPP1 concentration and glutathione peroxidase (GPX) activity, the latter due largely to the selenoprotein GPX3 secreted by the kidneys, were measured before and after supplementation. RESULTS: GPX activity was increased more by both doses of selenate than by the placebo in C-P class B patients. The activity was not increased more by selenomethionine supplementation than by the placebo in C-P class B patients. Plasma selenium was increased more by 400 μg Se as selenate than by the placebo in C-P class C patients. Within the groups who responded to selenate, there was a considerable variation in responses. CONCLUSION: These results indicate that severe cirrhosis causes mild functional selenium deficiency in some patients that is associated with impaired metabolism of selenomethionine. This trial was registered at clinicaltrials.gov as NCT00271245. SN - 1938-3207 UR - https://www.unboundmedicine.com/medline/citation/26468123/full_citation L2 - https://academic.oup.com/ajcn/article-lookup/doi/10.3945/ajcn.115.110932 DB - PRIME DP - Unbound Medicine ER -