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Journal of Nutrition Vol. 111 No. 12 December 1981, pp. 2106-2116
Copyright © 1981 by American Society for Nutrition
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Renal Acid, Urinary Cyclic AMP, and Hydroxyproline Excretion as Affected by Level of Protein, Sulfur Amino Acid, and Phosphorus Intake1

Sally A. Schuette2, Maren Hegsted, Michael B. Zemel and Hellen M. Linkswiler

Department of Nutritional Sciences, University of Wisconsin, Madison, WI 53706

Two 51-day human studies were conducted to investigate the effects of level of protein and phosphorus intake on the various components of renal acid excretion and on urinary sulfate, cyclic AMP and hydroxyproline; the role of the sulfur amino acids (Saa) of the protein was also evaluated. Dietary treatments included: 1) a 50 g protein diet; 2) a 150 g protein diet; and 3) a 50 g protein diet plus Saa to equal that of the 150 g protein diet, each given at 2 levels of phosphorus (1010 and 2525 mg). Calcium intake was 500 mg. Subjects were 16 young adult males. The results are discussed in relationship to calcium data previously reported (1, 2). Changes in renal acid and calcium excretion are not directly related for these reasons: a) the Saa accounted for all of the protein-induced increase in urinary sulfate and acid but for only 43% of the increase in urinary calcium and b) the acid phosphate supplement decreased urinary calcium but increased total acid excretion. The phosphorus supplement increased cyclic AMP but not hydroxyproline excretion. In fact, protein and Saa caused increases in hydroxyproline that were greatly reduced by the phosphorus supplement. Increases in urinary hydroxyproline and calcium were well correlated indicating that, at low calcium intakes, protein or Saa-induced increases in urinary calcium result in increased bone resorption which is reduced by the administration of phosphorus.


KEY WORDS: • dietary protein • dietary phosphorus • renal acid • urinary sulfate • cyclic AMP • hydroxyproline

1 Supported in part by the College of Agricultural and Life Sciences, University of Wisconsin, Madison, and by grant AM-19290, National Institute of Health, Bethesda, MD.

2 Current address is Department of Physiology, Milton S. Hershey Medical Center, Hershey, PA.

Manuscript received 29 April 1981.


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