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在仔猪出生后的早期发育阶段,十二指肠钙吸收不受骨化三醇的刺激。

Duodenal Ca2+ absorption is not stimulated by calcitriol during early postnatal development of pigs.

作者信息

Schroeder B, Dahl M R, Breves G

机构信息

Department of Physiology, School of Veterinary Medicine, D-30173 Hannover, Germany.

出版信息

Am J Physiol. 1998 Aug;275(2):G305-13. doi: 10.1152/ajpgi.1998.275.2.G305.

DOI:10.1152/ajpgi.1998.275.2.G305
PMID:9688658
Abstract

The role of calcitriol in stimulating intestinal active Ca2+ absorption during postnatal life was studied in newborn, suckling, and weaned control (Con) piglets and piglets suffering from inherited calcitriol deficiency (Def piglets). In addition, a group of Def piglets was treated with vitamin D3 (Def-D3 piglets), which normalized plasma calcitriol levels. Regardless of age, duodenal calbindin-D9k concentrations ranged between 1,839 and 2,846 microg/g mucosa in Con piglets, between 821 and 1,219 microg/g mucosa in Def piglets, and between 2,960 and 3,692 microg/g mucosa in Def-D3 animals. In weaned animals, active Ca2+ absorption as calculated from in vitro 45Ca2+ flux rate measurements in Ussing chambers could be related to calbindin-D9k levels. Thus active Ca2+ absorption was completely absent in Def animals but was reconstituted in Def-D3 animals. In contrast, in newborn Def piglets active Ca2+ absorption functioned normally despite the low plasma calcitriol and mucosal calbindin-D9k levels and could not be affected by treatment with vitamin D3. Similar results were obtained from suckling Def piglets. The microtubule-disrupting agent colchicine caused significant inhibition of transepithelial net Ca2+ absorption in duodenal epithelia from newborn piglets without exerting an effect in suckling and weaned animals. Colchicine had no effect on Ca2+ uptake across the brush border membrane of mucosal enterocytes or on glucose-dependent electrogenic net ion flux rates in duodenal preparations from newborn Con piglets. In conclusion, our findings reveal intestinal active Ca2+ absorption during early postnatal life of pigs that involves calcitriol-independent mechanisms and that may include intact microtubule actions.

摘要

在新生、哺乳和断奶的对照(Con)仔猪以及患有遗传性骨化三醇缺乏症的仔猪(Def仔猪)中,研究了骨化三醇在出生后刺激肠道主动吸收Ca2+的作用。此外,一组Def仔猪用维生素D3进行治疗(Def-D3仔猪),这使血浆骨化三醇水平恢复正常。无论年龄如何,Con仔猪十二指肠钙结合蛋白-D9k浓度在1839至2846μg/g黏膜之间,Def仔猪在821至1219μg/g黏膜之间,Def-D3动物在2960至3692μg/g黏膜之间。在断奶动物中,根据Ussing室中体外45Ca2+通量率测量计算出的主动Ca2+吸收与钙结合蛋白-D9k水平有关。因此,Def动物中完全没有主动Ca2+吸收,但在Def-D3动物中得以恢复。相反,新生Def仔猪尽管血浆骨化三醇和黏膜钙结合蛋白-D9k水平较低,但主动Ca2+吸收功能正常,且不受维生素D3治疗的影响。哺乳的Def仔猪也得到了类似的结果。破坏微管的药物秋水仙碱显著抑制了新生仔猪十二指肠上皮细胞的跨上皮净Ca2+吸收,而对哺乳和断奶动物没有影响。秋水仙碱对黏膜肠细胞刷状缘膜的Ca2+摄取或新生Con仔猪十二指肠制剂中葡萄糖依赖性电生性净离子通量率没有影响。总之,我们的研究结果揭示了猪出生后早期肠道主动吸收Ca2+的过程,该过程涉及不依赖骨化三醇的机制,可能包括完整的微管作用。

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