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首页> 外文期刊>American Journal of Physiology >Lack of the intestinal Muc1 mucin impairs cholesterol uptake and absorption but not fatty acid uptake in Muc1-/- mice.
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Lack of the intestinal Muc1 mucin impairs cholesterol uptake and absorption but not fatty acid uptake in Muc1-/- mice.

机译：缺乏肠道Muc1粘蛋白会损害Muc1-/-小鼠的胆固醇摄取和吸收，但不会损害脂肪酸的摄取。

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摘要

Before cholesterol and fatty acid molecules in the small intestinal lumen can interact with their possible transporters for uptake and absorption, they must pass through a diffusion barrier, which may modify the kinetics of nutrient assimilation. This barrier includes an unstirred water layer and a surface mucous coat, which is located at the intestinal lumen-membrane interface. In the present study, we investigated whether disruption of the mucin gene (Muc)1 may influence intestinal uptake and absorption of cholesterol and fatty acid in male Muc1(-/-) mice. The wild-type mice displayed relatively high levels of Muc1, Muc2, Muc3, and Muc4 mRNAs and relatively low levels of Muc5ac and Muc5b mRNAs in the small intestine. The absence of Muc1 mRNA and protein in the small intestines of Muc1(-/-) mice confirmed complete knockout of the Muc1 gene, but the mRNA expression for other mucin genes remained unchanged. Intestinal uptake and absorption of cholesterol but not palmitic acid were significantly reduced in Muc1(-/-) mice compared with the wild-type mice. However, knockout of the Muc1 gene did not impair either expression levels of the genes that encode intestinal sterol efflux transporters Abcg5 and Abcg8 and fatty acid transporter Fatp4 or small intestinal transit rates. We conclude that physiological levels of the epithelial mucin produced by the Muc1 gene are necessary for normal intestinal uptake and absorption of cholesterol in mice. Our study implies that because cholesterol absorption efficiency is reduced by approximately 50% in Muc1-deficient mice, there may be one or more additional pathways for cholesterol absorption.
机译：在小肠管腔中的胆固醇和脂肪酸分子可以与其可能的转运蛋白相互作用以吸收和吸收之前，它们必须穿过扩散屏障，这可能会改变营养物同化的动力学。该屏障包括未搅拌的水层和位于肠腔-膜界面的表面粘膜。在本研究中，我们调查了黏蛋白基因（Muc）1的破坏是否可能影响雄性Muc1（-/-）小鼠的肠道吸收以及胆固醇和脂肪酸的吸收。野生型小鼠在小肠中显示相对较高水平的Muc1，Muc2，Muc3和Muc4 mRNA，相对较低水平的Muc5ac和Muc5b mRNA。 Muc1（-/-）小鼠的小肠中缺少Muc1 mRNA和蛋白，证实完全敲除了Muc1基因，但其他粘蛋白基因的mRNA表达保持不变。与野生型小鼠相比，Muc1（-/-）小鼠的肠道摄取和吸收胆固醇而不是棕榈酸显着降低。但是，Muc1基因的敲除并不会损害编码肠道固醇外排转运蛋白Abcg5和Abcg8和脂肪酸转运蛋白Fatp4的基因的表达水平或小肠转运速率。我们得出结论，Muc1基因产生的上皮黏蛋白的生理水平对于正常肠道摄取和吸收小鼠胆固醇是必需的。我们的研究表明，由于在Muc1缺陷型小鼠中胆固醇吸收效率降低了约50％，因此可能存在一种或多种其他胆固醇吸收途径。

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