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ANGPTL8/贝塔托芬不能控制胰腺β细胞的扩张

Viktoria Gusarova¹, Corey A Alexa¹, Erqian Na¹

¹Regeneron Pharmaceuticals, Tarrytown, NY 10591, USA.

|November 24, 2014

概括

血管类蛋白8 (ANGPTL8) 不能控制胰腺β细胞的增殖. ANGPTL8影响甘油三水平,这表明其抑制可能治疗高甘油三.

科学领域:

代谢研究的研究.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

血管蛋白样蛋白8 (ANGPTL8) 最近被提议作为"贝塔洛芬",这是胰腺β细胞增殖的关键调节剂.
以前对Angptl8淘汰赛小鼠的研究表明,甘油三水平降低,但对葡萄糖平衡无影响.

研究的目的:

在胰岛素抵抗条件下研究ANGPTL8在胰腺β细胞扩张中的作用.
要确定ANGPTL8是否可以诱导β细胞的增殖或扩张.
探索ANGPTL8对血甘油三水平的影响.

主要方法:

在吃高脂肪饮食或接受胰岛素受体对抗剂治疗的Angptl8淘汰赛小鼠中对β细胞扩张的分析 (S961).
对小鼠肝脏特异性ANGPTL8过度表达的β细胞扩张和葡萄糖代谢的评估.
在淘汰赛和过度表达模型中测量血甘油三水平.

主要成果:

尽管诱导了胰岛素抵抗,但Angptl8淘汰小鼠表现出正常的β细胞扩张.
在小鼠肝脏中过度表达ANGPTL8并没有影响β细胞扩张或葡萄糖代谢.
ANGPTL8 删除显著降低了血甘油三水平,而过度表达则使其翻了一番.

结论:

ANGPTL8 在控制胰腺β细胞生长或扩张方面没有作用.
ANGPTL8显著影响血甘油三水平,这表明它在脂质代谢中起作用.
抑制ANGPTL8可能是管理高甘油三血症的潜在治疗策略.

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