Zhang Ke-Xin, Kan Cheng-Xia, Wang Yu-Qun, Hou Ning-Ning, Sun Xiao-Dong
Department of Endocrinology and Metabolism, The Affiliated Hospital of Shandong Second Medical University, Weifang 261031, Shandong Province, China.
World J Diabetes. 2024 Dec 15;15(12):2380-2383. doi: 10.4239/wjd.v15.i12.2380.
Type 1 diabetes (T1D) is characterized by the autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency and the need for exogenous insulin. A significant concern in T1D management is hypoglycemia, which is worsened by impaired counterregulatory mechanisms. Effective counterregulation involves hormones such as glucagon and adrenaline, which work to restore normal blood glucose levels. However, in T1D, these mechanisms often fail, particularly after recurrent hypoglycemia, resulting in hypoglycemia-associated autonomic failure. Recent research indicates that elevated levels of intestinal glucagon-like peptide-1 (GLP-1) impair counterregulatory responses by reducing the secretion of glucagon and adrenaline. This editorial underscores GLP-1's role beyond its incretin effects, contributing to impaired hypoglycemic counterregulation. This understanding necessitates a nuanced approach to GLP-1-based therapies in T1D, balancing the benefits of glycemic control with potential risks. Future research should delve into the mechanisms behind GLP-1's effects and explore potential interventions to improve hypoglycemic counterregulation. The goal is to enhance the safety and quality of life for T1D patients.
1型糖尿病（T1D）的特征是胰腺β细胞发生自身免疫性破坏，导致绝对胰岛素缺乏并需要外源性胰岛素。T1D管理中的一个重大问题是低血糖，而反调节机制受损会使低血糖情况恶化。有效的反调节涉及胰高血糖素和肾上腺素等激素，它们的作用是恢复正常血糖水平。然而，在T1D中，这些机制常常失效，尤其是在反复发生低血糖之后，会导致低血糖相关自主神经功能衰竭。最近的研究表明，肠道胰高血糖素样肽-1（GLP-1）水平升高会通过减少胰高血糖素和肾上腺素的分泌来损害反调节反应。这篇社论强调了GLP-1在其肠促胰岛素作用之外的作用，它会导致低血糖反调节受损。这种认识使得在T1D中对基于GLP-1的疗法采取细致入微的方法成为必要，要在血糖控制的益处与潜在风险之间取得平衡。未来的研究应该深入探究GLP-1作用背后的机制，并探索潜在的干预措施以改善低血糖反调节。目标是提高T1D患者的安全性和生活质量。
