SLC16a6,mTORC1和自调节肠道细胞中的体分泌
Takashi Uebanso1, Moeka Fukui1, Chisato Naito1
1Department of Preventive Environment and Nutrition, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima 770-8503, Japan.
肠道体的产生和分泌受营养的可用性和细胞过程的影响. 针对mTORC1-自途径和MCT7显示出调节肠道中这些关键代谢物的潜力.
科学领域:
- 生物化学 生化学
- 细胞生物学 细胞生物学
- 胃肠病学 胃肠病学
背景情况:
- 体在肠道健康中起着至关重要的作用,包括干细胞功能和癌症进展.
- 调节肠道类体度的机制尚不清楚.
研究的目的:
- 为了研究控制体生产和排泄在肠道细胞中的因素.
- 为了确定调节肠道体代谢的潜在治疗点.
主要方法:
- 在Caco2和HT29结直肠细胞系中利用了shRNA介导和药理抑制.
- 操纵培养基成分 (葡萄糖,酸盐,谷氨酸) 来模仿禁食条件.
- 评估了抑制mTORC1,自,巴西金和MCT7对体水平的影响.
主要成果:
- 禁食模仿媒介增加了体的酸生产和分泌,这种效应被葡萄糖或谷氨酸逆转.
- 抑制mTORC1部分恢复的排泄的体.
- 自抑制抑制了体的分泌.
- 基因倒置增加了体的分泌,同时降低了乳酸和酸盐的分泌.
- 在MCT7中,MCT7 knockdown显著减少了体的分泌.
结论:
- mTORC1-自轴是肠道体分泌的关键调节器.
- 单碳酸盐运输体7 (MCT7) 在肠道体分泌中起着至关重要的作用.
- mTORC1-自途径和MCT7是治疗性干预肠道代谢障碍的潜在目标.
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