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Selenium supplementation and insulin resistance in a randomized, clinical trial
  1. Elizabeth Theresa Jacobs1,2,3,
  2. Peter Lance2,4,
  3. Lawrence J Mandarino4,5,
  4. Nathan A Ellis2,
  5. H-H Sherry Chow2,
  6. Janet Foote1,
  7. Jessica A Martinez2,3,
  8. Chiu-Hsieh Paul Hsu1,2,
  9. Ken Batai6,
  10. Kathylynn Saboda2,
  11. Patricia A Thompson7
  1. 1 Department of Epidemiology and Biostatistics, Mel and Enid Zuckerman College of Public Health, University of Arizona, Tucson, Arizona
  2. 2 University of Arizona Cancer Center, Tucson, Arizona
  3. 3 Department of Nutritional Sciences, University of Arizona, Tucson, Arizona
  4. 4 Department of Medicine, University of Arizona, Tucson, Arizona
  5. 5 Center for Disparities in Diabetes, Obesity and Metabolism, University of Arizona, Tucson, Arizona
  6. 6 Department of Surgery, University of Arizona, Tucson, Arizona
  7. 7 Department of Medicine, Stony Brook University, New York City, New York, USA
  1. Correspondence to Dr Elizabeth Theresa Jacobs; jacobse{at}email.arizona.edu

Abstract

Objective While controversial, observational and randomized clinical trial data implicate the micronutrient selenium (Se) in the development of type 2 diabetes (T2D). The aim of this study was to test the hypothesis that Se supplementation adversely affects pancreatic β-cell function and insulin sensitivity.

Research design and methods In a subset of 400 individuals participating in a randomized, placebo-controlled trial of Se at 200 µg/day for colorectal adenomatous polyps, fasting plasma glucose and insulin were measured before randomization and within 6 months of completing intervention. Change in the homeostasis model assessment-β cell function (HOMA2-%β) and insulin sensitivity (HOMA2-%S) were compared between arms. A subgroup of 175 (79 Se and 96 placebo) participants underwent a modified oral glucose tolerance test (mOGTT) at the end of intervention and change in glucose values was assessed.

Results No statistically significant differences were observed for changes in HOMA2-%β or HOMA2-%S between those who received Se compared with placebo. After a mean of 2.9 years on study, mean HOMA2-%β values were 3.1±24.0 and 3.1±29.8 for the Se and placebo groups, respectively (p=0.99). For HOMA2-%S, the values were −0.5±223.2 and 80.9±1530.9 for the Se and placebo groups, respectively (p=1.00). Stratification by sex or age did not reveal any statistically significant effects on insulin sensitivity by treatment group. For mOGTT, mean baseline fasting blood glucose concentrations were significantly higher among participants in the placebo group compared with the Se group (96.6±14.6 and 92.3±12.0, respectively; p=0.04), a trend which remained through the 20 min assessment.

Conclusions These findings do not support a significant adverse effect of daily Se supplementation with 200 µg/day of selenized yeast on β-cell function or insulin sensitivity as an explanation for previously reported associations between Se and T2D. Further clarification of longer term effects of Se is needed.

Clinical trial registry NIH Clinical Trials.gov number NCT00078897.

  • selenium
  • supplementation
  • insulin resistance
  • HOMA
  • homeostatic model assessment
  • OGTT

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Footnotes

  • ETJ and PL contributed equally.

  • Contributors ETJ, PL, LJM, H-HSC, and ETJ were responsible for the initial design of the project, as well as data collection. C-HPH, ETJ, and KS were responsible for conducting the data analyses. NAE, JF, JAM, C-HPH, and KB made key contributions to the preparation of the manuscript, specifically in interpretation of the data. All authors participated in the writing of the manuscript and have approved it in its final form for submission.

  • Funding Financial Support: the National Cancer Institute Cancer Center Support Grant P30 CA023074, NIH/NCI R01CA151708 (ETJ), NIH/NCI P01 CA041108 (PL); NIH R01DK047396 (LJM) and NIH/NCI R01CA151708 (PL).

  • Competing Interests None declared.

  • Patient consent for publication Not required.

  • Ethics approval The University of Arizona Institutional Review Board (IRB) approved and oversaw the study protocol.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Data requests should be directed to ETJ at jacobse@email.arizona.edu. Deidentified data included in this work may be obtained through an established process. A data request form will be supplied for completion and approval by the authors the manuscript. Reuse is permitted for reasonable, scientifically rigorous research.

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