• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Peripheral and central regulation of insulin by the intestine and microbiome
【24h】

Peripheral and central regulation of insulin by the intestine and microbiome

机译：肠道和微生物组的外周和中枢调节胰岛素

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Blood glucose and insulin homeostasis is disrupted during the progression of type 2 diabetes. Insulin levels and action are regulated by both peripheral and central responses that involve the intestine and microbiome. The intestine and its microbiota process nutrients and generate molecules that influence blood glucose and insulin. Peripheral insulin regulation is regulated by gut-segment-dependent nutrient sensing and microbial factors such as short-chain fatty acids and bile acids that engage G-protein-coupled receptors. Innate immune sensing of gut-derived bacterial cell wall components and lipopolysaccharides also alter insulin homeostasis. These bacterial metabolites and postbiotics influence insulin secretion and insulin clearance in part by altering endocrine responses such as glucagon-like peptide-1. Gut-derived bacterial factors can promote inflammation and insulin resistance, but other postbiotics can be insulin sensitizers. In parallel, activation of small intestinal sirtuin 1 increases insulin sensitivity by reversing high fat-induced hypothalamic insulin resistance through a gut-brain neuronal axis, whereas high fat-feeding alters small intestinal microbiome and increases taurochenodeoxycholic acid in the plasma and the dorsal vagal complex to induce insulin resistance. In summary, emerging evidence indicates that intestinal molecular signaling involving nutrient sensing and the host-microbe symbiosis alters insulin homeostasis and action. Gut-derived host endocrine and paracrine factors as well as microbial metabolites act on the liver, pancreas, and the brain, and in parallel on the gut-brain neuronal axis. Understanding common nodes of peripheral and central insulin homeostasis and action may reveal new ways to target the intestinal host-microbe relationship in obesity, metabolic disease, and type 2 diabetes.
机译：在2型糖尿病的进展过程中，血糖和胰岛素稳态被破坏。胰岛素水平和作用由涉及肠道和微生物组的外周和中枢反应调节。肠道及其微生物群处理营养物质并产生影响血糖和胰岛素的分子。外周胰岛素调节受肠段依赖性营养传感和微生物因子的调节，如短链脂肪酸和胆汁酸，它们与G蛋白偶联受体结合。肠源性细菌细胞壁成分和脂多糖的先天免疫感应也会改变胰岛素稳态。这些细菌代谢物和益生素部分通过改变内分泌反应（如胰高血糖素样肽-1）影响胰岛素分泌和胰岛素清除。肠源性细菌因子可促进炎症和胰岛素抵抗，但其他益生元可能是胰岛素增敏剂。同时，激活小肠sirtuin 1可通过肠-脑神经轴逆转高脂诱导的下丘脑胰岛素抵抗，从而提高胰岛素敏感性，而高脂喂养可改变小肠微生物群，并增加血浆和迷走神经背侧复合体中的牛磺脱氧胆酸，从而诱导胰岛素抵抗。总之，新的证据表明，涉及营养感应和宿主微生物共生的肠道分子信号改变了胰岛素的稳态和作用。肠道来源的宿主内分泌和旁分泌因子以及微生物代谢产物作用于肝脏、胰腺和大脑，并平行作用于肠道-大脑神经元轴。了解外周和中枢胰岛素稳态和作用的共同节点，可能会揭示针对肥胖、代谢性疾病和2型糖尿病中肠道-宿主-微生物关系的新方法。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号