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在饮食诱导的肥胖小鼠中,新型肠导向小分子GPR119激动剂的慢性代谢作用

Mohan Patil¹, Dinesh Thapa¹, Leon N Warne²

¹Curtin Medical School and Curtin Health Innovation Research Institute, Curtin University, Bentley, Perth, WA 6102, Australia.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

|November 20, 2024

概括

新型GPR119激动剂与西塔利普丁结合,改善了肥胖小鼠的葡萄糖控制和减轻体重增加. 组合疗法也显著改善了肝硬化症,显示出治疗代谢功能障碍相关的肝硬化性肝炎的潜力.

科学领域:

药理学药理学是指药理学的学科.
代谢疾病代谢疾病
肝病学肝病学是一种肝病学.

背景情况:

G蛋白结合受体-119 (GPR119) 的激活影响葡萄糖,能量和脂质代谢,与2型糖尿病 (T2D) 有关.
开发针对胃肠道受体的合成小分子GPR119激动剂为代谢障碍提供了治疗策略.

研究的目的:

在高脂肪饮食诱导的肥胖 (DIO) 小鼠中研究新型GPR119激动剂 (ps297,ps318) 的慢性代谢作用.
评估单独和与西塔格利平素 (DPP-IV抑制剂) 结合使用这些激动剂在改善代谢功能障碍和肝硬化方面的疗效.

主要方法:

DIO小鼠接受了为期10周的口服治疗,单独使用GPR119激动剂 (10-90 mg/kg/天) 或使用西塔利普丁 (20 mg/kg/天).
监测了代谢参数,包括体重,食物摄入量,血糖和葡萄糖耐受性.
治疗后评估了肝脏生物标志物,肝脏肥胖症标志物 (甘油三,胆固醇) 和组织病理学.

主要成果:

与西塔利普丁的联合治疗恢复了因克雷丁和胰岛素分泌,改善了葡萄糖平衡,并减少了体重增加.
通过减少肝脏重量,酶和炎症,GPR119激素单独治疗改善了肝脏健康.
组合疗法进一步增强了肝脏效应,显著降低了肝脏肥胖症标志物,并改善了他的病理学发现.

结论:

新型肠导向的GPR119激动剂在治疗代谢功能障碍方面显示出治疗潜力.
结合DPP-IV抑制剂,如西塔格利普丁,可能提供一种协同方法来改善与代谢功能障碍相关的脂肪肝炎 (MASH).
需要进一步的机制研究来充分阐明治疗效益.

关键词:

这是一种DPP-IV抑制剂.肝脏肥胖症肝脏肥胖症肥胖问题肥胖问题合成的GPR119激活剂是一种激活剂.2 型糖尿病 2 型糖尿病

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