胰高血糖素在肥胖治疗中的复兴
本文是《柳叶刀·糖尿病与内分泌学》评论，探讨胰高血糖素在肥胖治疗中的角色转变。胰高血糖素曾因在2型糖尿病中驱动高血糖而被视为抑制靶点，现通过GLP-1平衡共激动剂被有意利用，以发挥其更广泛的代谢作用而不损害血糖控制。该评论强调其在禁食和能量需求增加时协调能量稳态，包括促进肝脏脂肪酸β氧化、生酮、氨基酸分解代谢和尿素生成，并增加能量消耗。
要点
- 胰高血糖素从抑制靶点转变为治疗靶点，与GLP-1平衡共激动剂用于肥胖治疗。
- 平衡共激动可发挥胰高血糖素代谢益处，同时不损害血糖控制。
- 胰高血糖素促进脂肪酸β氧化、生酮、氨基酸分解代谢和尿素生成，增加能量消耗。
核心结论
- 胰高血糖素在肥胖治疗中复兴，通过GLP-1平衡共激动剂利用其代谢作用，且不损害血糖控制。
主要发现
- 胰高血糖素从抑制靶点转变为被刻意利用的治疗靶点。
以上解读依据论文摘要（全文未开放获取或许可不允许翻译转载）。
原文
Few hormones have undergone such a profound therapeutic reappraisal as glucagon. Long regarded as a therapeutic target for inhibition because of its central role in driving hyperglycaemia in type 2 diabetes, glucagon is now being deliberately harnessed through balanced co-agonism with GLP-1, allowing its broader metabolic actions to be therapeutically exploited without compromising glycaemic control.1,2 Beyond stimulating hepatic glucose production, glucagon coordinates energy homeostasis during fasting and increased energy demand by promoting hepatic fatty acid β oxidation, ketogenesis, amino-acid catabolism, and ureagenesis, in addition to increasing energy expenditure through mechanisms that remain incompletely understood.
引用
- The Lancet Diabetes and Endocrinology：[Comment] The glucagon renaissance in obesity therapeutics
供执业医师工作参考，不替代临床判断；数值与分级以指南原文为准。