Bar, A., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Striem, S., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Mayel-Afshar, S., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel
Lawson, D.E.M., Institute of Animal Science, Agricultural Research Organization, Volcani Center, Bet Dagan, Israel

The effect of shell calcification and 1,25-dihydroxy-vitamin D3 (1,25-(OH)2D3) on calbindin-D(28K) (previously known as vitamin D-dependent calcium-binding protein) and calbindin mRNA was investigated in the intestine and eggshell gland (ESG) of juvenile female chicks, laying hens and non-laying female birds with active gonads. Increasing amounts of 1,25-(OH)2D3 were fed to laying hens and juvenile birds treated with oestradiol to develop the ESG. The intestinal concentration of calbindin was increased 30-fold by 1,25-(OH)2D3 in chicks treated with oestradiol and fed a vitamin D-deficient diet. In these same animals, 1,25-(OH)2D3 had no effect on the formation of calbindin mRNA or calbindin in the ESG even though fully viable 1,25-(OH)2D3 receptors are present in this tissue. In laying birds fed adequate amounts of vitamin D3, intestinal, but not ESG, calbindin was increased by the addition of 1,25-(OH)2D3 to the diet. At the onset of egg production the concentrations of calbindin and calbindin mRNA were increased in the intestine and ESG. This increase occurred within the period of calcification of the first egg, through a process unaffected by vitamin D. Calcification of the first egg increased the concentration of calbindin in the ESG by eight- to tenfold, although the concentration of calbindin mRNA was increased by only two- to threefold. These results suggest that the induction of calbindin synthesis by 1,25-(OH)2D3 or by the egg calcification process is associated with an increase in the concentration of calbindin mRNA in the ESG and in testine. They also suggest that the vitamin D-dependent physiological changes in the ESG occurring during the calcification process do not include an increase in calbindin synthesis, that calbindin is induced and/or regulated by a mechanism requiring additional factors besides 1,25-(OH)2D3, and that post-transcriptional regulation of calbindin synthesis in these tissues may be possible.