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Zinc Nutritional Status Modulates the Response of 1,25-Dihydroxycholecalciferol to Calcium Depletion in Rats¹

Paul L. Kimmel, Christopher T. Gubish, Don W. Watkins^* and Craig B. Langman

Rita Gusack Laboratory, Department of Medicine ^* Department of Physiology, George Washington University Medical Center, Washington, DC 20037 Mineral Metabolism Laboratory, Department of Pediatrics, Northwestern University and Children's Memorial Hospital, Chicago, IL 60614

Male Lewis rats (n = 27) were fed a non-purified diet containing 0.9% calcium, 0.7% phosphorus, and 0.005% zinc until 8 wk of age. At this time rats were assigned randomly to one of two groups. Both groups were fed a low calcium, low zinc, purified diet (0.2% calcium, 0.4% phosphorus, <0.00007% zinc), but one group was fed 1.78 mg Zn/(animal·d). The zinc-replete animals were individually matched by weight to the zinc-depleted animals and pair-fed. Balances and plasma concentrations of zinc, calcium, and phosphorus and parathyroid hormone, 25 hydroxycholecalciferol [25(OH)D] and 1,25-dihydroxycholecalciferol [1,25(OH)₂D] were determined at the start of calcium depletion and 2 wk later. Calcium and 25(OH)D levels were lower in both groups after calcium depletion. Dietary zinc had no significant effect on calcium or 25(OH)D levels. Phosphorus concentrations were lower after calcium depletion, but phosphorus concentration was higher in the zinc-depleted compared with the zinc-replete group at the end of the experiment. 1,25(OH)₂D increased in both groups, but was higher in the zinc-replete than the zinc-depleted group at the end of the experiment. Calcium and phosphorus balances were greater in the zinc-depleted group at the end of the experiment. We conclude zinc depletion diminishes the response of 1,25(OH)₂D to calcium depletion in rats. The mechanism is unknown, but may involve nonhormonally mediated changes in gastrointestinal absorption of calcium and phosphorus or an affect of zinc on extraintestinal processes.

KEY WORDS: • calcitriol • parathyroid hormone • vitamin D • phosphorus • rats

¹ Supported by grants from the National Capital Chapter, National Kidney Foundation, and the BRSG program of the National Institutes of Health (BRSG RR05359-25) (PLK), and by grants DK33949 and AR30692 from the National Institutes of Health and a grant from the Otto Sprague Memorial Fund (CBL).

Manuscript received 15 November 1991. Revision accepted 18 February 1992.