DIETARY-PROTEIN AFFECTS INTESTINAL CALCIUM-ABSORPTION

Citation
Je. Kerstetter et al., DIETARY-PROTEIN AFFECTS INTESTINAL CALCIUM-ABSORPTION, The American journal of clinical nutrition, 68(4), 1998, pp. 859-865
Citations number
41
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00029165
Volume
68
Issue
4
Year of publication
1998
Pages
859 - 865
Database
ISI
SICI code
0002-9165(1998)68:4<859:DAIC>2.0.ZU;2-A
Abstract
Background: Changes in dietary protein in adults are associated with c hanges in urinary calcium excretion. The mechanisms underlying this ef fect are not completely understood, but alterations in intestinal abso rption of calcium are not thought to be involved. Objective: We reexam ined this mechanism by evaluating the effect of 2 amounts of dietary p rotein (low: 0.7 g/kg; and high: 2.1 g/kg) on fractional calcium absor ption in 7 healthy, young women. Design: The experiment consisted of 2 wk of a well-balanced diet containing moderate amounts of calcium, so dium, and protein followed by 5 d of an experimental diet that contain ed 1 of 2 amounts of protein and constant amounts of other nutrients k nown to influence calcium metabolism. Seven subjects received both amo unts of dietary protein in random order. Blood and urine were sampled at baseline and on day 4. Fractional calcium absorption was measured b y dual-stable calcium isotopes on day 5. In a second study of 5 additi onal women, we evaluated the effects of dietary fiber on calcitropic h ormones. Results: Subjects developed hypocalciuria and secondary hyper parathyroidism on day 4 of the low-protein diet. Urinary calcium excre tion and the glomerular filtration rate were elevated significantly by day 4 of the high-protein compared with the low-protein diet. Fractio nal calcium absorption after the low-protein diet was 0.19 +/- 0.03, w hich was significantly lower than that after the high-protein diet (0. 26 +/- 0.03, P = 0.05). Conclusion: These data provide evidence that d epressed intestinal calcium absorption explains, in part, low-protein- induced secondary hyperparathyroidism.