Abstract：
Glucose and energy metabolism disorders are the main reasons induced type 2 diabetes (T2D) and obesity. Besides providing energy, dietary nutrients could regulate glucose homeostasis and food intake via intestinal nutrient sensing induced gut hormone secretion. However, reviews regarding intestinal protein sensing are very limited, and no accurate information is available on their underlying mechanisms. Through intestinal protein sensing, dietary proteins regulate glucose homeostasis and food intake by secreting gut hormones, such as glucagon-like peptide 1 (GLP-1), cholecystokinin (CCK), peptide YY (PYY) and glucose-dependent insulinotropic polypeptide (GIP). After activating the sensory receptors, such as calcium-sensing receptor (CaSR), peptide transporter-1 (PepT1), and taste 1 receptors (T1Rs), protein digests induced Ca2+ influx and thus triggered gut hormone release. Additionally, research models used to study intestinal protein sensing have been emphasized, especially several innovative models with excellent physiological relevance, such as co-culture cell models, intestinal organoids, and gut-on-a-chips. Lastly, protein-based dietary strategies that stimulate gut hormone secretion and inhibit gut hormone degradation are proposed for regulating glucose homeostasis and food intake.
摘要：
葡萄糖和能量代谢紊乱是导致2型糖尿病(T2D)和肥胖的主要原因。除了提供能量，膳食营养素可以通过肠道营养感知诱导的肠道激素分泌来调节葡萄糖稳态和食物摄入。然而,关于肠道蛋白传感的评论非常有限，并且没有关于其基本机制的准确信息。通过肠道蛋白质传感，膳食蛋白质通过分泌肠道激素调节葡萄糖稳态和食物摄入，如胰高血糖素样肽1（GLP-1），胆囊收缩素(CCK),肽YY(PYY)和葡萄糖依赖性促胰岛素多肽(GIP)。激活感觉感受器后，如钙敏感受体（CaSR），肽转运蛋白-1（PepT1），和味觉1受体（T1R），蛋白质消化诱导Ca2+内流，从而触发肠道激素释放。此外,强调了用于研究肠道蛋白质传感的研究模型，特别是几个具有优异生理相关性的创新模型，例如共培养细胞模型，肠道类器官，和芯片上的肠道。最后,提出了刺激肠道激素分泌和抑制肠道激素降解的基于蛋白质的饮食策略，用于调节葡萄糖稳态和食物摄入。
