Krieger Jean-Philippe, Daniels Derek, Lee Shin, Mastitskaya Svetlana, Langhans Wolfgang
Vetsuisse Faculty, Institute of Veterinary Pharmacology and Toxicology, University of Zurich, Zurich, Switzerland.
Institute of Neuroscience and Physiology, University of Gothenburg, Gothenburg, Sweden.
Compr Physiol. 2025 Feb;15(1):e7. doi: 10.1002/cph4.7.
Glucagon-like peptide-1 (GLP-1), a hormone released from enteroendocrine cells in the distal small and large intestines in response to nutrients and other stimuli, not only controls eating and insulin release, but is also involved in drinking control as well as renal and cardiovascular functions. Moreover, GLP-1 functions as a central nervous system peptide transmitter, produced by preproglucagon (PPG) neurons in the hindbrain. Intestinal GLP-1 inhibits eating by activating vagal sensory neurons directly, via GLP-1 receptors (GLP-1Rs), but presumably also indirectly, by triggering the release of serotonin from enterochromaffin cells. GLP-1 enhances glucose-dependent insulin release via a vago-vagal reflex and by direct action on beta cells. Finally, intestinal GLP-1 acts on the kidneys to modulate electrolyte and water movements, and on the heart, where it provides numerous benefits, including anti-inflammatory, antiatherogenic, and vasodilatory effects, as well as protection against ischemia/reperfusion injury and arrhythmias. Hindbrain PPG neurons receive multiple inputs and project to many GLP-1R-expressing brain areas involved in reward, autonomic functions, and stress. PPG neuron-derived GLP-1 is involved in the termination of large meals and is implicated in the inhibition of water intake. This review details GLP-1's roles in these interconnected systems, highlighting recent findings and unresolved issues, and integrating them to discuss the physiological and pathological relevance of endogenous GLP-1 in coordinating these functions. As eating poses significant threats to metabolic, fluid, and immune homeostasis, the body needs mechanisms to mitigate these challenges while sustaining essential nutrient intake. Endogenous GLP-1 plays a crucial role in this "ingestive homeostasis."
胰高血糖素样肽-1(GLP-1)是一种由远端小肠和大肠的肠内分泌细胞在对营养物质和其他刺激作出反应时释放的激素,它不仅控制进食和胰岛素释放,还参与饮水控制以及肾脏和心血管功能。此外,GLP-1作为一种中枢神经系统肽递质,由后脑的前胰高血糖素(PPG)神经元产生。肠道GLP-1通过GLP-1受体(GLP-1Rs)直接激活迷走感觉神经元来抑制进食,但推测也通过触发肠嗜铬细胞释放血清素来间接抑制进食。GLP-1通过迷走-迷走反射和对β细胞的直接作用增强葡萄糖依赖性胰岛素释放。最后,肠道GLP-1作用于肾脏以调节电解质和水的运动,并作用于心脏,在心脏中它具有多种益处,包括抗炎、抗动脉粥样硬化和血管舒张作用,以及对缺血/再灌注损伤和心律失常的保护作用。后脑PPG神经元接收多种输入并投射到许多表达GLP-1R的脑区,这些脑区参与奖赏、自主功能和应激。PPG神经元衍生的GLP-1参与大餐的终止,并与水摄入的抑制有关。这篇综述详细阐述了GLP-1在这些相互关联系统中的作用,突出了最近的发现和未解决的问题,并将它们整合起来讨论内源性GLP-1在协调这些功能中的生理和病理相关性。由于进食对代谢、液体和免疫稳态构成重大威胁,身体需要机制来减轻这些挑战,同时维持必需营养物质的摄入。内源性GLP-1在这种“摄食稳态”中起着至关重要的作用。