Impaired duodenal response to short-term dietary calcium restriction in adolescent spontaneously hypertensive rats

Abstract

The response pattern of plasma calcitriol level and related intestinal adaptation to short-term moderate calcium (Ca) restriction was examined in adolescent male, spontaneously hypertensive rats (SHR) and normotensive WKY control rats. Twelve-week-old SHR and WKY fed a low (0.1%) Ca diet for 3, 6, or 12 days were compared with rats of either strain fed a normal (1.0%) Ca diet. Plasma calcitriol response was measured and duodenal adaptation to Ca restriction was investigated by evaluating active Ca transport, calbindin-D9K (CaBP9K) protein, CaBP9K mRNA, and alkaline phosphatase activity (ALP). Under the normal Ca diet, no significant difference between strains was observed for all five parameters. In response to the low Ca diet, the SHR and WKY showed a similar increase (nearly 50%) in plasma calcitriol, starting at day 3 of this diet. However, only the WKY displayed the expected duodenal adaptation: active Ca transport increased at day 6 and CaBP9K as well as ALP increased at day 3 of the low Ca diet. The stimulation of the latter three parameters was maintained until day 12 of Ca restriction. Moreover, CaBP9K mRNA was increased in WKY after 3 days of Ca restriction. In contrast, the SHR had either no or only a minor increase of duodenal parameters in response to Ca restriction. Finally, a significant and positive correlation between Ca transport and plasma calcitriol and between Ca transport and CaBP9K was found in WKY but not in SHR.(ABSTRACT TRUNCATED AT 250 WORDS)

Luminal calcium concentration controls intestinal calcium absorption by modification of intestinal alkaline phosphatase activity

“…The lack of statistical differences in Phe effect on %Ca with normal or high Ca intake could be explained, as in this situation, the enzyme would be, at least in part, stimulated by the luminal Ca concentration because Ca and Phe act on IAP activity in an opposite way; therefore, the inhibitory effect of Phe would not be as effective as in the group with low Ca intake. The increase in %Ca in the group with low Ca intake cannot be explained by the increase in protein expression as an adaptation to dietary Ca content, as demonstrated in a previous study ( 22 ) . Previously, it has been demonstrated that although calbindin expression and calcitriol levels were modified after 3 d of low Ca intake, the active duodenal Ca transport remained unchanged, which is consistent with our experiment.…”