Merrill J. Christensen and Dr. Brian Johnson, Food Science and Nutrition
Introduction Selenium (Se) is an essential trace mineral needed by the body in extremely small amounts. The main sources of Se in the diet are vegetables and meats. Selenium is incorporated in the enzyme Glutathione Peroxidase (GPx). GPx is an antioxidant that scavenges hydrogen peroxide and other organic peroxides to protect the body from oxidative damage.
Selenium has also been found to be incorporated into another enzyme called type I 5’iodothyronine deiodinase (ID1). This enzyme converts the thyroid hormone Thyroxine (T4) to its active form of tri-iodothyronine (T3) (1). Thyroid hormones have an overall effect on body metabolism. If these hormone concentrations are high, body metabolism goes up, and when they are low, metabolism is slowed down.
It has been shown that when Se is deficient in the diet, ID1 gene expression and activity are significantly decreased (2). As a result, blood T4 and thyroid stimulating hormone (TSH) concentrations increase and T3 concentrations decrease. The overall effect of Selenium deficiency is a reduction in body metabolism.
Little is known about the effects of an increased amount of selenium on thyroid hormone levels. Thyroid hormone levels can affect body composition, but no report has been submitted describing the effects of selenium on body composition.
Objective and Application
The objective of the project was to further examine the relationship of selenium and thyroid hormones with respect to body metabolism. To accomplish this, Body composition was assessed on male Sprague-Dawley rats fed different levels and forms of selenium in their diet. Body composition was then correlated to the animal’s respective selenium status and to its thyroid hormone levels.
Obesity is a major problem in America today. Body weight and composition is determined in part by thyroid hormones and their metabolism. If selenium affects thyroid hormone metabolism, then selenium may play a role in the regulation of body weight.
Materials and Methods
One hundred eight weanling male Sprague-Dawley rats were housed in pairs in hanging wire cages in a temperature- and light-controlled room. Rats were fed, in groups of 20 or more, one of five Torula Yeast Based diets: Se-deficient diet, 0.15 mg Se/Kg diet as sodium selenite or as sodium selenate (control Se diets), or supplemented with 2.0 mg Se/kg diet as sodium selenite or as sodium selenate (elevated Se diets). At thirteen weeks, the animals were measured for body composition using a computerized unit called EM-Scan. EM-Scan measures total body electrical conductivity (TOBEC), which is a useful 154 tool for comparing relative body fat measurements from one group to another. At fifteen weeks, animals were killed and Liver GPx activity was assessed to determine selenium status. GPx activity and body composition was then compared using analysis of variance. All procedures related to the care and use of experimental animals were approved by the BYU Institutional Animal Care and Use Committee.
Results and Conclusion
Activity of cellular GPx was measured, and as predicted, almost no GPx activity was reported in the Se-deficient animals, while the other Se-supplemented groups reported normal activity. This confirms a deficit of selenium in the Se-deficient animals.
Percent body fat and conductivity was then compared to each experimental group. It was found that the mean of animals deficient in Se was significantly different from that of any Se-supplemented group. There were no differences among the Se-supplemented groups. When comparing the nasoanal length among groups, no significant difference was found. This means that animals fed a Sedeficient diet had the same length compared to other groups, yet had a higher percent body fat. This data also suggest that an increased amount of selenium in the diet does not contribute to a decrease in percent body fat.
The finding of increased percent body fat in Se-deficient rats is consistent with the known effects of Se intake on thyroid hormone metabolism(3). ID1 gene expression and activity is significantly decreased in Se-deficient animals. These reductions are also associated with a reduction in T3 and an increase in T4 tissue and plasma concentrations. These data suggest that a selenium deficiency may produce a mild hypothyroid state in rats in which increased adiposity, as it is in humans, is characteristic.
A more detailed report of these findings, in conjunction with other results from the same study, were presented in the Federation of American Societies for Experimental Biology (FASEB) convention (April 18-22 1998, San Francisco, Ca.). These results have also been compiled and await publication (4).
References
- Berry, M. J., P. R. Larsen, “Molecular cloning of the selenocysteine-containing enzyme type I iodothyronine deiodinase.” American Journal of Clinical Nutrition 57:249s-255s, 1993.
- Arthur, J. R., et al, “Selenium deficiency, thyroid hormone metabolism, and thyroid hormone deiodinase.” American Journal of clinical Nutrition 57:236s-239s, 1993.
- Christensen, M. J., et al, “Tissue specificity of selenoprotein gene expression in rats.” Journal of Nutritional Biochemistry 6:367-372, 1995.
- Many thanks to Dr. Christensen, ORCA, and all others in the lab, who have helped me with my project.