Nys Y, Baker K, Bouillon R, Van Baelen H, Lawson D E
INRA Centre de Tours-Nouzilly, Monnaie, France.
Gen Comp Endocrinol. 1992 Jun;86(3):460-8. doi: 10.1016/0016-6480(92)90071-q.
Intestinal calbindin synthesis in laying hens was analyzed to assess controlling factors operating during egg formation. In the absence of vitamin D, calbindin was not induced by estrogen and testosterone. In immature vitamin D-replete pullet, blood levels of 1,25(OH)2D3 increased in response to estrogen but the duodenal concentration of calbindin and its mRNA were increased only when testosterone was given together with estrogen. The plasma concentration of 1,25(OH)2D3 and the duodenal levels of calbindin and its mRNA were substantially higher in laying hens than in immature pullets. No differences in these parameters were observed between the stages of the ovulatory cycle. Suppression of shell formation for a week decreased the concentration of 1,25(OH)2D3 and of duodenal calbindin but did not affect the level of its mRNA. When egg shell formation resumed in hens previously laying shell-less eggs, the concentrations of 1,25(OH)2D3 and of calbindin and its mRNA increased toward the end of shell formation. A most important factor regulating intestinal calbindin synthesis in laying hens turned out to be 1,25(OH)2D3. Intestinal calbindin mRNA is more stable in laying hens than in young birds as its concentration declines more slowly when the stimulation provided by 1,25(OH)2D3 is withdrawn, as occurs following suppression of shell formation and after parathyroidectomy in laying birds. Intestinal calbindin mRNA is therefore increased by a process other than increasing 1,25(OH)2D3 formation. The factor influencing the stability of this mRNA in laying hens could be calcium. It is concluded that in hens the increased duodenal calbindin synthesis elicited by plasma 1,25(OH)2D3 at sexual maturity primarily involves a transcriptional process and the stabilization of the mRNA.(ABSTRACT TRUNCATED AT 250 WORDS)
分析了蛋鸡肠道钙结合蛋白的合成，以评估在产蛋过程中起作用的控制因素。在缺乏维生素D的情况下，雌激素和睾酮不会诱导钙结合蛋白的产生。在维生素D充足的未成熟小母鸡中，1,25(OH)2D3的血液水平会因雌激素而升高，但只有当睾酮与雌激素一起给予时，十二指肠中钙结合蛋白及其mRNA的浓度才会升高。产蛋母鸡血浆中1,25(OH)2D3的浓度以及十二指肠中钙结合蛋白及其mRNA的水平显著高于未成熟小母鸡。在排卵周期的各个阶段，这些参数没有差异。抑制蛋壳形成一周会降低1,25(OH)2D3和十二指肠钙结合蛋白的浓度，但不影响其mRNA的水平。当先前产无壳蛋的母鸡恢复蛋壳形成时，1,25(OH)2D3、钙结合蛋白及其mRNA的浓度在蛋壳形成末期会升高。结果表明，调节蛋鸡肠道钙结合蛋白合成的一个最重要因素是1,25(OH)2D3。与幼鸟相比，蛋鸡肠道钙结合蛋白mRNA更稳定，因为当1,25(OH)2D3的刺激被撤除时，其浓度下降得更慢，如在抑制蛋壳形成后以及产蛋鸡甲状旁腺切除后发生的情况。因此，肠道钙结合蛋白mRNA的增加是通过增加1,25(OH)2D3形成以外的过程实现的。影响蛋鸡中这种mRNA稳定性的因素可能是钙。得出的结论是，在母鸡中，性成熟时血浆1,25(OH)2D3引起的十二指肠钙结合蛋白合成增加主要涉及转录过程和mRNA的稳定化。（摘要截短至250字）
