The Biochemical Indices of Experimental Phosphorus Depletion (PD): A Re-Examination of Their Physiological Implications
The biochemical features observed in experimental phosphorus (P) depletion include hypercalcemia (↑P-Ca), hypophosphatemia (↓P-P), hypercalciuria (↑U-Ca), hypophosphaturia (↓U-P) and intestinal calcium (Ca) hyperabsorption (1–7). Exogenous P deprivation is the usual mode of inducing PD and has been considered fundamental in the generation of the various biochemical changes (Figure 1). However, it is entirely reasonable to postulate that these changes also may be induced or aborted by modifying the metabolic need for P. In the present study we observed that normal young rats maintained on normal P diets may develop biochemical features of PD if they undergo unusual and spontaneous acceleration in growth. On the other hand, in young rats with growth arrest induced by hypophysectomy, both the biochemical and clinical changes caused by low P diet may either be aborted or attenuated. These findings stress the importance of defining the prevailing anabolic need of experimental animals in interpreting both the adequacy of dietary P and the significance of the clinical and the biochemical changes of PD. Some relevant examples will be discussed. We also provide evidence demonstrating that in young rats PD results in a net reduction in intestinal Ca retention. Since both the synthesis of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and its accumulation in intestinal mucosa are increased in P deprived rats (8,9), this finding may represent an example in which the physiological interrelationship between the activity of 1,25(OH)2D3 and net intestinal Ca retention is dissociated.
KeywordsPhosphorus Cage Thyroxine Hypercalcemia Rickets
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