Abstract：
BACKGROUND: This study aimed to investigate the impact of Vitamin A (VA) on intestinal glucose metabolic phenotypes.
METHODS: Male C57BL/6 mice were randomized assigned to a VA-normal diet (VAN) or a VA-deficient diet (VAD) for 12 weeks. After12 weeks, the VAD mice were given 30 IU/g/d retinol for 10 days and VAN diet (VADN) for 10 weeks. By using glucose tolerance tests, immunofluorescence staining, quantitative polymerase chain reaction, siRNA transduction, and enzyme-linked immunosorbent assay, the glucose metabolic phenotypes as well as secretory function and intracellular hormone changes of STC-1 were assessed.
RESULTS: VAD mice showed a decrease of glucose-stimulated insulin secretion and a loss of intestinal glucagon-like peptide-1 (GLP-1) expression. Through reintroducing dietary VA to VAD mice, the intestinal VA levels, GLP-1 expression and normal glucose can be restored. The incubation with retinol increased VA signaling factors expression within STC-1 cells, especially retinoic acid receptor β (RARβ). The activation of RARβ restored intracellular incretin hormone synthesis and secretory function.
CONCLUSIONS: VA deficiency leads to an imbalance of intestinal glucose metabolic phenotypes through a mechanism involving RARβ signaling pathway, suggesting a new method to achieve the treatment for VAD induced glucose metabolism impairment.
METHODS: Male C57BL/6 mice were randomized assigned to a VA-normal diet (VAN) or a VA-deficient diet (VAD) for 12 weeks. After12 weeks, the VAD mice were given 30 IU/g/d retinol for 10 days and VAN diet (VADN) for 10 weeks. By using glucose tolerance tests, immunofluorescence staining, quantitative polymerase chain reaction, siRNA transduction, and enzyme-linked immunosorbent assay, the glucose metabolic phenotypes as well as secretory function and intracellular hormone changes of STC-1 were assessed.
RESULTS: VAD mice showed a decrease of glucose-stimulated insulin secretion and a loss of intestinal glucagon-like peptide-1 (GLP-1) expression. Through reintroducing dietary VA to VAD mice, the intestinal VA levels, GLP-1 expression and normal glucose can be restored. The incubation with retinol increased VA signaling factors expression within STC-1 cells, especially retinoic acid receptor β (RARβ). The activation of RARβ restored intracellular incretin hormone synthesis and secretory function.
CONCLUSIONS: VA deficiency leads to an imbalance of intestinal glucose metabolic phenotypes through a mechanism involving RARβ signaling pathway, suggesting a new method to achieve the treatment for VAD induced glucose metabolism impairment.
摘要：
背景：本研究旨在研究维生素A（VA）对肠道葡萄糖代谢表型的影响。
方法:将雄性C57BL/6小鼠随机分配至VA正常饮食(VAN)或VA缺乏饮食(VAD)12周。12周后,给予VAD小鼠30IU/g/d视黄醇10天，VAN饮食(VADN)10周。通过使用葡萄糖耐量测试，免疫荧光染色，定量聚合酶链反应，siRNA转导,和酶联免疫吸附测定，评估了STC-1的葡萄糖代谢表型以及分泌功能和细胞内激素变化。
结果：VAD小鼠表现出葡萄糖刺激的胰岛素分泌减少和肠胰高血糖素样肽-1（GLP-1）表达丧失。通过将饮食VA重新引入VAD小鼠，肠道VA水平，GLP-1的表达和正常的葡萄糖可以恢复。与视黄醇孵育可增加VA信号因子在STC-1细胞内的表达，特别是视黄酸受体β（RARβ）。RARβ的激活恢复了细胞内肠促胰岛素激素的合成和分泌功能。
结论：VA缺乏通过涉及RARβ信号通路的机制导致肠道葡萄糖代谢表型失衡，提示一种新的方法来实现对VAD诱导的糖代谢障碍的治疗。
方法:将雄性C57BL/6小鼠随机分配至VA正常饮食(VAN)或VA缺乏饮食(VAD)12周。12周后,给予VAD小鼠30IU/g/d视黄醇10天，VAN饮食(VADN)10周。通过使用葡萄糖耐量测试，免疫荧光染色，定量聚合酶链反应，siRNA转导,和酶联免疫吸附测定，评估了STC-1的葡萄糖代谢表型以及分泌功能和细胞内激素变化。
结果：VAD小鼠表现出葡萄糖刺激的胰岛素分泌减少和肠胰高血糖素样肽-1（GLP-1）表达丧失。通过将饮食VA重新引入VAD小鼠，肠道VA水平，GLP-1的表达和正常的葡萄糖可以恢复。与视黄醇孵育可增加VA信号因子在STC-1细胞内的表达，特别是视黄酸受体β（RARβ）。RARβ的激活恢复了细胞内肠促胰岛素激素的合成和分泌功能。
结论：VA缺乏通过涉及RARβ信号通路的机制导致肠道葡萄糖代谢表型失衡，提示一种新的方法来实现对VAD诱导的糖代谢障碍的治疗。
