ARS | Publication request: SILICON DEFICIENCY AFFECTS URINARY INDICATORS OF BONE BREAKDOWN DIFFERENTLY IN OVARIECTOMIZED AND OVARY-INTACT RATS

Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract Only
Publication Acceptance Date: December 2, 2002
Publication Date: March 14, 2003
Citation: Nielsen, F.H. 2003. Silicon deficiency affects urinary indicators of bone breakdown differently in overiectomized and ovary-intact rats [abstract]. The Federation of American Societies for Experimental Biology Journal. 17:A706.

Technical Abstract: Silicon might have a function that affects the cell-to-cell communication, or cell signaling, role of one or more extracellular maxtrix glycoprotein/s involved in bone mineralization and wound healing. To ascertain the veracity of this suggestion, groups of 10 female weanling rats were used in a factorially arranged experiment with variables of supplemental dietary silicon (Si) at 0 or 35 mg/kg, and ovariectomy (alters bone formation and turnover) or sham-operation at the start of the experiment. The basal diet contained about 2 mg Si/kg. Silicon deprivation for 6 weeks increased urinary deoxypyridinoline in ovary-intact rats, but not in ovariectomized rats. Both Si deficiency and ovariectomy significantly increased urinary helical peptide; the effect of ovariectomy was most marked in Si-supplemented rats. Sham-operated rats fed 35 mg Si/kg diet had the lowest urinary excretion of pyridinoline, deoxypyridinoline and helical peptide expressed per mmol of creatinine. Plasma sialic acid was increased while plasma osteopontin was decreased by Si deprivation for 8 weeks. Both plasma sialic acid and osteopontin were decreased by ovariectomy. These findings support the hypothesis that silicon has an essential function that affects bone formation and turnover, and possibly involves the interaction between the extracellular matrix glycoprotein osteopontin (a sialoprotein) and its cell-surface receptor.