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膳食钙缺乏会增加雏鸡肠上皮细胞对钙离子的摄取和钙离子的外排机制。

Dietary calcium deficiency increases Ca2+ uptake and Ca2+ extrusion mechanisms in chick enterocytes.

作者信息

Centeno Viviana A, Díaz de Barboza Gabriela E, Marchionatti Ana M, Alisio Arturo E, Dallorso Maria E, Nasif Renée, Tolosa de Talamoni Nori G

机构信息

Laboratorio de Metabolismo Fosfocálcico y Vitamina D "Dr. F. Cañas", Cátedra de Bioquímica y Biología Molecular, Facultad de Ciencias Médicas, Universidad Nacional de Córdoba, Argentina.

出版信息

Comp Biochem Physiol A Mol Integr Physiol. 2004 Oct;139(2):133-41. doi: 10.1016/j.cbpb.2004.08.002.

DOI:10.1016/j.cbpb.2004.08.002
PMID:15528161
Abstract

Ca2+ uptake and Ca2+ extrusion mechanisms were studied in enterocytes with different degree of differentiation from chicks adapted to a low Ca2+ diet as compared to animals fed a normal diet. Chicks adapted to a low Ca2+ diet presented hypocalcemia, hypophosphatemia and increased serum 1,25(OH)2D3 and Ca2+ absorption. Low Ca2+ diet increased the alkaline phosphatase (AP) activity, independently of the cellular maturation, but it did not alter gamma-glutamyl-transpeptidase activity. Ca2+ uptake, Ca2+-ATPase and Na(+)/Ca2+ exchanger activities and expressions were increased by the mineral-deficient diet either in mature or immature enterocytes. Western blots analysis shows that vitamin D receptor (VDR) expression was much higher in crypt cells than in mature cells. Low Ca2+ diet decreased the number of vitamin D receptor units in both kinds of cells. In conclusion, changes in Ca2+ uptake and Ca2+ extrusion mechanisms in the enterocytes by a low Ca2+ diet appear to be a result of enhanced serum levels of 1,25(OH)2D3, which would promote cellular differentiation producing cells more efficient to express vitamin D dependent genes required for Ca2+ absorption.

摘要

研究了适应低钙饮食的雏鸡与正常饮食喂养的动物相比,不同分化程度肠细胞中的钙离子摄取和钙离子外排机制。适应低钙饮食的雏鸡出现低钙血症、低磷血症,血清1,25(OH)₂D₃和钙离子吸收增加。低钙饮食增加了碱性磷酸酶(AP)活性,与细胞成熟无关,但未改变γ-谷氨酰转肽酶活性。无论是成熟还是未成熟的肠细胞,低钙饮食均增加了钙离子摄取、钙离子ATP酶和钠/钙交换器的活性及表达。蛋白质免疫印迹分析表明,维生素D受体(VDR)在隐窝细胞中的表达远高于成熟细胞。低钙饮食降低了两种细胞中维生素D受体单位的数量。总之,低钙饮食引起的肠细胞钙离子摄取和钙离子外排机制的变化似乎是血清1,25(OH)₂D₃水平升高的结果,这将促进细胞分化,产生更高效表达钙离子吸收所需维生素D依赖性基因的细胞。

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