VITAMIN D AND CALCIUM DURING LACTATION

研究的总体目标是：a）描述 调节肠道钙吸收和甲状旁腺 泌乳期间的激素分泌和B）表征 调节1，25- 二羟维生素D3在哺乳期和新生儿期。 肠钙吸收的调节将通过以下方式确定： a）测量活性钙转运（使用外翻的肠囊， 体外）和维生素D依赖性钙离子的含量， 大鼠十二指肠和回肠中的9 KD CaBP结合蛋白 在怀孕和哺乳期间，和B）测量不饱和的 空肠和回肠中的钙转运（具有外翻肠囊 和Ussing室）。 待检验的假设 （1）哺乳期十二指肠CaBP和主动钙转运 不依赖于1，25-（OH）2D 3，但受催乳素刺激，或 另一种与哺乳有关的激素，（2）不饱和钙 泌乳期间空肠和回肠的转运增强 由于哺乳介导的肠道结构变化， 上皮 甲状旁腺激素（PTH）分泌将 通过测定a）血浆PTH水平 通过N末端特异性放射免疫测定法（RIA），和B） 甲状旁腺细胞体外释放PTH的速率 哺乳期大鼠使用骨肉瘤细胞cAMP生物测定PTH。 促胰液素和皮质酮在增强免疫反应中的作用 哺乳期PTH分泌将通过体外PTH检测 释放程序，以及吸吮刺激和 空腹/再喂养将通过血浆PTH的RIA测定。 的 结果可能揭示了参与的因素以外， 低钙血症在维持血浆PTH水平升高中的作用 哺乳期 哺乳期1，25-（OH）_2D_3合成的调控 出生后的发育将由肾脏25- 0 HD 3 -1-羟化酶测定。 由于大鼠血浆1，25-（OH）2D 3 幼崽在2至5周龄之间显著增加，而 血浆PTH没有变化，建议血浆中的升高 1，25-（OH）2D 3在此期间是由于增加的敏感性， 肾25-OHD 3 -1-羟化酶活性对PTH。 的 对哺乳期大鼠的拟议研究可能表明催乳素的作用 刺激肾脏25-OHD 3 -1-羟化酶。 的结果 拟议的研究将揭示调节因素和适应性 当钙的需求量增加时， 哺乳期母亲和哺乳期婴儿的 和刚断奶的孩子

The general objectives of the research are to a) characterize the regulation of intestinal calcium absorption and parathyroid hormone secretion during lactation and b) characterize the regulation of synthesis and circulating levels of 1, 25- dihydroxyvitamin D3 during lactation and the neonatal period. Regulation of intestinal calcium absorption will be determined by a) measuring active calcium transport (using everted gut sacs in vitro) and the content of the vitamin D-dependent calcium- binding protein (9 KD CaBP) in the duodenum and ileum of rats during pregnancy and lactation, and b) measuring nonsaturable calcium transport in the jejunum and ileum (with everted gut sacs and Ussing chambers) of lactating rats. Hypotheses to be tested are: (1) duodenal CaBP and active calcium transport in lactation are independent of 1, 25-(OH)2D3 but stimulated by prolactin or another lactation-related hormone, (2) nonsaturable calcium transport in the jejunum and ileum is enhanced during lactation because of lactation-mediated structural changes in the intestinal epithelium. Parathyroid hormone (PTH) secretion will be examined during lactation by determining a) the plasma PTH level by an N-terminal-specific radioimmunoassay (RIA), and b) the rate of release of PTH in vitro from parathyroid cells from lactating rats using an osteosarcoma cell cAMP bioassay for PTH. The potential roles of secretin and corticosterone in enhancing PTH secretion during lactation will be tested by the in vitro PTH release procedure, and the effects of the suckling stimulus and fasting/refeeding will be determined by RIA of plasma PTH. The results may reveal the involvement of factors other than hypocalcemia in maintaining elevated plasma PTH levels during lactation. The control of 1, 25-(OH)2D3 synthesis during lactation and postnatal development will be determined by a renal 25- OHD3-1-hydroxylase assay. Since plasma 1,25-(OH)2D3 in rat pups increases markedly between 2 and 5 weeks of age, while plasma PTH does not change, it is proposed that the rise in plasma 1, 25-(OH)2D3 during this period is due to increasing sensitivity of the renal 25-OHD3-1-hydroxylase enzyme activity to PTH. The proposed work with lactating rats may indicate a role of prolactin in stimulating the renal 25-OHD3-1-hydroxylase. The results of the proposed studies will reveal regulatory factors and adaptive mechanisms that come into play when calcium demands are increased markedly for both the lactating mother and the suckling and newly weaned offspring.