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  • Title: Nutritional interrelationships between calcium, phosphorus and lactose in rats.
    Author: Schaafsma G, Visser R.
    Journal: J Nutr; 1980 Jun; 110(6):1101-11. PubMed ID: 7381583.
    Abstract:
    From the age of 3 months, six groups of rats consisting of six animals each were fed one of three types of diet with either 15% lactose or dextrose. The diets used were a control diet containing 0.6% calcium and 0.45% phosphorus and two high-phosphorus (1.3%) diets with either a normal (0.6%) or a low (0.2%) calcium content. Whereas calcium retention and femur mass appeared to be unaffected, feeding the high-phosphorus diets resulted in significant (P less than or equal to 0.05 or P less than or equal to 0.01) biochemical changes including: decreased plasma phosphorus almost throughout the whole of the study; increased plasma alkaline phosphatase, and urinary total hydroxyproline after 17 and 42 weeks; nephrocalcinosis; depressed urinary calcium, and reduced femur density. With the excretion of nephrocalcinosis and depressed urinary calcium, these changes were more marked if the calcium content of the diet was low than when it was normal, and this difference was associated with a significant (P less than 0.01) inhibiting effect of dietary calcium on the intestinal absorption and urinary excretion of phosphorus. Although lactose, as compared with dextrose, significantly (P less than 0.01) improved the intestinal absorption and retention of calcium during body weight gain, which was reflected by an increased femur mass after 42 weeks, this sugar did not reduce the detrimental effects on bone and soft tissue resulting from feeding the high-phosphorus diets. The results of the study in line with the induction of nutritional secondary hyperparathyroidism and increased bone turnover in rats fed high-phosphorus diets and indicate that lactose-stimulated calcium absorption will not prevent or diminish the biochemical changes associated with this disease; the results also stress the significance of the calcium content of the diet as a factor that may protect the body against excessive dietary phosphorus.
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