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-CoA结合蛋白用于厌食症的实验性治疗

Hui Chen^1,2,3, Stéphanie Moriceau⁴, Adrien Joseph^1,5

¹Centre de Recherche des Cordeliers, Equipe labellisée par la Ligue contre le cancer, Inserm U1138, Université Paris Cité, Sorbonne Université, 75006 Paris, France.

Science translational medicine

|August 14, 2024

概括

细胞外乙-辅酶A结合蛋白 (ACBP/DBI) 的低水平与神经性厌食症有关. 在小鼠中补充ACBP/DBI可以预防由压力或化疗引起的厌食症,这表明一种潜在的治疗方法.

科学领域:

神经科学是一个神经科学.
内分泌学在内分泌学.
分子生物学分子生物学

背景情况:

细胞外乙-辅酶A结合蛋白 (ACBP/DBI) 是一种通过自分泌的食欲兴奋剂.
低ACBP/DBI血水平与神经性厌食症患者的预后不佳相关.
在小鼠中,压力诱导的厌食症减少了循环的ACBP/DBI.

研究的目的:

为了研究ACBP/DBI补充剂用于厌食症的治疗潜力.
开发一种控制ACBP/DBI分泌的方法.
阐明ACBP/DBI在预防厌食症中的机制.

主要方法:

在转基因小鼠中设计了一种化学遗传系统,用于生物可激活,自独立的ACBP/DBI分泌.
通过化学遗传系统,静脉注射或透给药ACBP/DBI.
通过慢性克制压力 (CRS) 或化疗药物 (cisplatin, doxorubicin, paclitaxel) 评估厌食症诱导.
测量了血利波卡林-2度和下丘脑黑色皮质素4受体的激活.

主要成果:

在小鼠中,生物素诱导的ACBP/DBI升高预防了CRS或化疗引起的厌食症.
ACBP/DBI逆转了CRS/cisplatin诱导的利波卡林-2和下丘脑厌食信号的增加.
重组ACBP/DBI管理模仿了这些氧化作用.

结论:

细胞外ACBP/DBI补充剂是一种有前途的厌食症治疗策略.
针对ACBP/DBI可能为神经性厌食症和化疗诱导的厌食症提供一种新的治疗方法.
ACBP/DBI可能会抵消涉及利波卡林-2的厌食性途径.

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