BIO5 Institute, University of Arizona, Tucson, AZ, USA.
School of Animal and Comparative Biomedical Sciences, University of Arizona, Tucson, AZ, USA.
Nat Commun. 2021 Feb 10;12(1):903. doi: 10.1038/s41467-021-21235-y.
The gastrointestinal tract maintains energy and glucose homeostasis, in part through nutrient-sensing and subsequent signaling to the brain and other tissues. In this review, we highlight the role of small intestinal nutrient-sensing in metabolic homeostasis, and link high-fat feeding, obesity, and diabetes with perturbations in these gut-brain signaling pathways. We identify how lipids, carbohydrates, and proteins, initiate gut peptide release from the enteroendocrine cells through small intestinal sensing pathways, and how these peptides regulate food intake, glucose tolerance, and hepatic glucose production. Lastly, we highlight how the gut microbiota impact small intestinal nutrient-sensing in normal physiology, and in disease, pharmacological and surgical settings. Emerging evidence indicates that the molecular mechanisms of small intestinal nutrient sensing in metabolic homeostasis have physiological and pathological impact as well as therapeutic potential in obesity and diabetes.
胃肠道通过营养感应和随后向大脑和其他组织发出信号来维持能量和葡萄糖内稳态。在这篇综述中，我们强调了小肠营养感应在代谢内稳态中的作用，并将高脂肪喂养、肥胖和糖尿病与这些肠道-大脑信号通路的紊乱联系起来。我们确定了脂质、碳水化合物和蛋白质如何通过小肠感应途径从肠内分泌细胞中引发肠肽释放，以及这些肽如何调节食物摄入、葡萄糖耐量和肝葡萄糖生成。最后，我们强调了肠道微生物群如何影响正常生理和疾病、药理学和手术环境中的小肠营养感应。新出现的证据表明，代谢内稳态中小肠营养感应的分子机制在肥胖和糖尿病中具有生理和病理影响以及治疗潜力。
