|Nielsen, Forrest - Frosty|
|Poellot, Rhonda Lee|
Submitted to: Journal of Trace Elements in Experimental Medicine
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/15/2003
Publication Date: 7/26/2004
Citation: Nielsen, F.H., Poellot, R.A. 2004. Dietary silicon affects bone turnover differently in ovariectomized and sham-operated growing rats. Journal of Trace Elements in Experimental Medicine. 17:137-149. Interpretive Summary: Because dietary restriction of silicon leads to undesirable changes in experimental animals, including defective bone growth and joint cartilage formation, silicon possibly is an essential nutrient for humans. General acceptance of silicon essentiality, however, will require identification of a clearly defined biochemical function for the element in higher animals and humans. Apparent deficiency signs described for experimental animals suggest that silicon has a function that affects the action of proteins known as extracellular matrix glycoproteins involved in cell-to-cell communication, cell adhesion, and cell signaling that are needed for cells to develop so that form joint cartilage and a matrix upon which bone is formed. Thus, an experiment was performed to see whether low dietary silicon would affect blood and bone concentrations of some of these proteins and thus affect bone strength and shape. Half of the rats also had their ovaries removed which made them estrogen-deficient and impairs bone formation. Findings were obtained suggesting that silicon has a biochemical function that can affect blood and bone concentrations of some extracellular matrix proteins, the activity of some enzymes associated with bone formation, the excretion of bone and joint cartilage breakdown products, and the response to estrogen deficiency. Surprisingly, these effects of silicon did not markedly affect bone calcium content or bone breaking characteristics. This indicates that silicon does not have a major effect on bone crystal formation or function once mineralization has been initiated, but has an effect on bone growth processes prior to this process and at sites other than in bone. Silicon apparently is needed for normal bone organic matrix and joint cartilage formation and this need can be altered by estrogen deficiency. Thus, an inadequate intake of silicon possibly can contribute to the risk of becoming osteoarthritic or osteoporotic.
Technical Abstract: An experiment was performed to test the hypothesis that low dietary silicon affects blood, bone, and urine indices associated with bone formation and breakdown, and bone strength and physical characteristics, and the circulating amount of an extracellular matrix protein (osteopontin) involved in bone cell adhesion and activation. A second objective was to ascertain whether ovariectomy (estrogen deficiency) alters the effects of low dietary silicon on bone formation. 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 or 35 mg/kg, and ovariectomy (estrogen-deficient) or sham-operation at the start of the experiment. The basal silicon-low diet contained about 2 mg Si/kg. Low dietary silicon compared to adequate silicon decreased plasma osteopontin concentration, increased plasma sialic acid concentration, and increased urinary helical peptide excretion. Low dietary silicon also affected the response to estrogen deficiency. Ovariectomy increased plasma alkaline phosphatase in the silicon-supplemented, but not in the silicon-low rats. In contrast, ovariectomy decreased liver ornithine aminotransferase in silicon-low but not in silicon-supplemented rats. Ovariectomy increased the urinary excretion of deoxypyridinoline and decreased the femur concentration of sialic acid more markedly in silicon-supplemented than silicon-low rats. Silicon and an interaction between silicon and ovariectomy only mildly changed bone strength and physical measurements and did not affect femur calcium concentration. The findings suggest that silicon has a biochemical function that affects bone growth processes prior to bone crystal formation by affecting bone collegan turnover and sialic acid-containing extracellular matrix proteins such as osteopontin.