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肝脏受损的极低密度脂蛋白分泌促进瘤发生,并通过Fabp1删除加速

Elizabeth P Newberry¹, Elizabeth A Molitor¹, Allen Liu¹

¹Department of Medicine, Washington University School of Medicine, St. Louis, Missouri.

The American journal of pathology

|February 28, 2024

概括

极低密度脂蛋白 (VLDL) 分泌受损促进小鼠肝癌. 阻断脂肪酸结合蛋白1 (Fabp1) 矛盾地加速了瘤生长和死亡率,突出了肝脏瘤发生中的复杂代谢作用.

科学领域:

肝病学和癌症生物学肝病学和癌症生物学
脂质新陈代谢和运输
分子遗传学分子遗传学

背景情况:

极低密度脂蛋白 (VLDL) 分泌受损与肝脏疾病有关,包括肥胖症,纤维化和肝细胞癌.
肝脏特异性微体甘油三转移蛋白淘汰 (Mttp-LKO) 的小鼠会发生肝硬化和纤维化,而Mttp-LKO X Fabp1-null (Fabp1/Mttp双重淘汰,DKO) 的小鼠则会减少肝硬化和纤维化.

研究的目的:

研究受损VLDL分泌对肝细胞癌 (HCC) 发病率和进展的影响.
为了比较Mttp-LKO小鼠与Fabp1/Mttp DKO小鼠中的HCC发育情况.

主要方法:

甲基氨酸 (DEN) 治疗用于诱导Mttp-LKO和Fabp1/Mttp DKO小鼠的肝细胞癌症.
分析包括瘤负担评估,死亡率,血清脂质概况,内阿波利波蛋白表达,肝脂组学和RNA测序.
使用葡萄糖和谷氨酸利用量测试来评估肝细胞代谢能力.

主要成果:

与对照组相比,Mttp-LKO小鼠在经过DEN治疗后表现出肥胖症和瘤负担的增加.
在Fabp1/Mttp DKO小鼠中,瘤负担异常增加,死亡率显著上升.
观察到高密度脂蛋白胆固醇的升高,三糖类物种的改变,能量代谢的转变 (有氧糖解,葡萄糖/谷氨酸利用),以及减少HNF1本体箱A (HNF1a) 表达,与瘤负担相关.

结论:

损伤的VLDL分泌增强了肝脏瘤发生.
在受损VLDL分泌的背景下,Fabp1功能的丧失通过复杂的代谢变化加速HCC的进展和死亡率.
改变脂肪酸细分和肝脏能量利用途径对于调节肝细胞癌症的发展至关重要.

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