1alpha-hydroxycholecalciferol does not increase the specific activity of intestinal phytase but does improve phosphorus utilization in both cecectomized and sham-operated chicks fed cholecalciferol-adequate diets.

Two chick assays were conducted in an attempt to understand how 1alpha-hydroxylated cholecalciferol compounds [1,25-(OH)2 D3 and 1alpha-OH D3] function in chicks to improve utilization of phytate-bound phosphorus (P) and trace minerals. Mucosal tissue from chicks fed a P-deficient corn-soybean meal diet, with or without supplemental 1alpha-OH D3, was incubated with sodium phytate. Inorganic P (Pi) release from sodium phytate, a measure of mucosal phytase activity, was not influenced by 1alpha-OH D3 presence in the diet. Increasing doses of mucosal protein in tubes containing sodium phytate resulted in marked increases (P < 0.01) in Pi release, but 1alpha-OH D3 in the diet from which the duodenal mucosal tissue was obtained had no effect on Pi release. Similarly, addition of either 1alpha-OH D3 or 1,25-(OH)2 D3 directly to the incubation tubes had no effect on Pi production. Efficacy of supplemental 1alpha-OH D3 and phytase was also tested in cecectomized vs. sham-operated chicks that were fed P-deficient and cholecalciferol-adequate corn-soybean meal diets. Removal of the twin ceca was done in an attempt to remove much of the intestinal microbial activity, and in turn, much of the gut microbial phytase activity. Marked increases (P < 0.01) in bone ash occurred in response to phytase or 1alpha-OH D3 supplementation, and cecectomized birds responded to either addition in the same manner as sham-operated controls. The data suggest that the marked phytate-P releasing capacity of dietary 1alpha-OH D3 or 1, 25-(OH)2 D3 is not caused by an increased specific activity of intestinal phytase.