Abstract

We studied 28 healthy premenopausal women before and after manipulating Ca intake, and then in response to a hypercalcemic challenge. Women with low Ca intakes at entry (< 17.5 mmol/day) were restricted to about 5 mmol/day (low-Ca), and those with higher self-selected intakes were supplemented to about 70 mmol/d (high-Ca). After 8 weeks on these regimens, more bone resorption was occurring among the low-Ca women, as evidenced by their higher values for immunoreactive PTH and urine hydroxyproline. There was a 7-fold range in 24-h urine Ca among the low-Ca women, with upper values equivalent to about 80% of intake. In response to induced hypercalcemia (0.5 mmol Ca/kg lean body mass, infused over 4 h), the low-Ca group had greater increases in serum Ca (1.31 vs. 1.05 mmol/L, P < 0.05) and reached a marginally higher peak (3.64 vs. 3.50 mmol/L, P < 0.1). Despite these greater calcemic responses, the low-Ca women excreted a smaller fraction of the infused Ca (44.3 vs. 62.2%, P < 0.02). Furthermore, preinfusion urine Ca was directly correlated with excretion of infused Ca in the low-Ca women, but not in the high-Ca women. Preinfusion differences between groups in immunoreactive PTH and urine hydroxyproline tended to reappear within 2 days. Our findings show that there are detectable differences in the Ca regulatory system between subjects at practical extremes of Ca intake, and that these differences persist through exposure to a temporary Ca surfeit. Ca-restricted women have higher levels of PTH and of bone remodeling activity. There is considerable variation in the apparent capacity to conserve Ca among women with low intakes. None of our subjects had high-P diets. Thus, our findings show that Ca restriction can evoke a persistent PTH response in the absence of a high P intake.

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