Luminal glucose does not enhance active intestinal calcium absorption in mice: evidence against a role for Ca(v)1.3 as a mediator of calcium uptake during absorption.
Luminal glucose does not enhance active intestinal calcium absorption in mice: evidence against a role for Ca(v)1.3 as a mediator of calcium uptake during absorption.
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DOI：
10.1016/j.nutres.2015.08.004
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发表时间：
2015-11
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影响因子：
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通讯作者：
Fleet JC
中科院分区：
文献类型：
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作者：
Reyes-Fernandez PC;Fleet JC
肠道钙吸收通过1，25（OH）2D 3调节的跨细胞途径发生，特别是当习惯性膳食钙摄入量低时。最近，L-型电压门控钙通道，Cav1.3，提出了介导主动，跨细胞钙吸收的膜去极化引起的升高的管腔葡萄糖水平餐后。我们测试了高管腔葡萄糖可以揭示Cav1.3在小鼠主动肠钙吸收中的作用的假设。9周龄雄性C57 BL/6 J小鼠饲喂含低（0.125%）或高（1%）Ca的AIN 93 G饲料1周，并通过口服灌胃法使用含25 mmol/L葡萄糖或果糖的45 Ca转运缓冲液检测Ca吸收。测定了十二指肠、空肠和回肠中瞬时受体电位香草酸6（TRPV 6）、钙结合蛋白D9 k（CaBPD 9 k）和Cav1.3 mRNA的水平。TRPV 6和CaBPD 9 k表达在十二指肠中最高，其中发生活性的1，25（OH）2D 3调节的Ca吸收，而Cav1.3 mRNA水平在整个肠段中相似。正如预期的那样，低钙饮食使肾脏细胞色素p450- 27 B1（CYP 27 B1）mRNA（p=0.003）、血清1，25（OH）2D 3（p<0.001）和果糖缓冲液的钙吸收效率增加2倍。然而，用于促进Cav1.3激活的葡萄糖缓冲液不增加钙吸收效率（p=0.6），无论饮食钙摄入水平如何。总的来说，我们的研究结果表明，葡萄糖没有增强钙的吸收，他们不支持Cav1.3在基础或维生素D调节的肠道钙吸收体内的关键作用。
Intestinal Ca absorption occurs through a 1,25 dihydroxyvitamin D3 (1,25(OH)2D3)-regulated transcellular pathway, especially when habitual dietary Ca intake is low. Recently the L-type voltage-gated Ca channel, Cav1.3, was proposed to mediate active, transcellular Ca absorption in response to membrane depolarization caused by elevated luminal glucose levels following a meal. We tested the hypothesis that high luminal glucose could reveal a role for Cav1.3 in active intestinal Ca absorption in mice. Nine week-old male C57BL/6J mice were fed AIN93G diets containing either low (0.125%) or high (1%) Ca for 1 week and Ca absorption was examined by an oral gavage method using a 45Ca-transport buffer containing 25 mmol/L of glucose or fructose. Transient receptor potential vanilloid 6 (TRPV6), Calbindin D9k (CaBPD9k) and Cav1.3 mRNA levels were measured in the duodenum, jejunum and ileum. TRPV6 and CaBPD9k expression were highest in the duodenum, where active, 1,25(OH)2D3-regulated Ca absorption occurs while Cav1.3 mRNA levels were similar across the intestinal segments. As expected, the low Ca diet increased renal cytochrome p450-27B1 (CYP27B1) mRNA (p=0.003), serum 1,25(OH)2D3 (p<0.001) and Ca absorption efficiency by 2-fold with the fructose buffer. However, the glucose buffer used to favor Cav1.3 activation did not increase Ca absorption efficiency (p=0.6) regardless of the dietary Ca intake level. Collectively, our results show that glucose did not enhance Ca absorption and they do not support a critical role for Cav1.3 in either basal or vitamin D-regulated intestinal Ca absorption in vivo.