Submitted to: Workshop Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 9/14/2002
Publication Date: 10/18/2002
Citation: Nielsen, F.H. 2002. Silicon nutrition affects urinary and plasma indicators of bone and connective tissue metabolism. In: Anke, M., Muller, R., Schafer, U., Stoeppler, M., editors. Macro and Trace Elements. Friedrich Schiller University, Jena, Germany, October 18-19, 2002. Leipzig, Germany:Schubert-Verlag. p.1231-1237.
Interpretive Summary: Because dietary restriction of silicon leads to undesirable changes in experimental animals, including defective bone growth and mineralization initiation, silicon possibly is an essential element for humans. General acceptance of silicon as essential, however, will require identification of a clearly defined biochemical function for the element in higher animals and humans. Silicon may have a function that affects the interaction between proteins known as extracellular matrix glycoproteins involved in cell-to-cell communication, and signaling to cells to perform certain functions such as bone mineralization. One of these proteins known as osteopontin has been shown to be involved in the regulation of most functions affected by silicon deficiency, including the mineralization of bone. Thus, an experiment was done with female rats that were fed silicon deficient or supplemented diets. Half of the rats on each diet also had their ovaries removed, which impairs normal bone formation. Urine was collected after six weeks and blood was obtained after 8 weeks of feeding. Urine markers of bone breakdown were increased, while plasma osteopontin was decreased, by both silicon deficiency and removal of ovaries. The finding that ovariectomy and silicon deficiency had similar effects on these measurements supports the suggestion that silicon has an essential function in bone formation and maintenance, and this function is related to the function of osteopontin. Thus, an adequate intake of silicon may be part of a nutritional program for bone health.
Technical Abstract: An experiment was performed with the objectives of confirming that silicon status affects bone formation and turnover, and to test the hypothesis that silicon status can affect the interaction between one or more extracellular matrix glycoprotein/s and cell-surface receptors to alter the circulating amount of these glycoproteins, and turnover of type I collagen. Female rats weighing about 56 g were assigned to groups of 10 in a factorially arranged experiment. The variables were supplemental dietary silicon at 0 and 35 mg/kg, and undergoing ovariectomy and sham-operation procedures at the start of the experiment. The basal silicon-deficient diet contained about 2 mg Si/kg. Silicon deprivation for six weeks affected urinary variables indicative of bone resorption, but the nature of some effects were dependent upon the presence of an intact ovary. Urinary deoxypyridinoline was increased by silicon deficiency in ovary-intact rats, but decreased by silicon deficiency in ovariectomized rats. Urinary pyridinoline tended to show a similar response to silicon and ovariectomy. Both silicon deficiency and ovariectomy significantly increased urinary helical peptide, with the effect of ovariectomy most marked in silicon-adequate rats. Plasma sialic acid was increased while osteopontin was decreased by silicon deprivation for eight weeks. Both plasma sialic acid and osteopontin were decreased by the removal of the ovaries. These findings support the hypothesis that silicon functions to affect the actions of extracellular matrix glycoproteins, thus affecting bone formation and turnover.