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荷艾氏腹水瘤小鼠肿瘤细胞和组织中脂蛋白脂肪酶活性(LPLA)的变化

Changes in lipoprotein lipase activity (LPLA) in tumor cells and tissues in mice bearing Ehrlich ascites tumor.

作者信息

Bálint Z, Holczinger L

出版信息

Bull Cancer. 1984;71(5):412-8.

PMID:6525466
Abstract

Lipid content and lipoprotein lipase activity (LPLA) of serum and various tissues of mice bearing Ehrlich ascites tumor have been studied. The growing tumor caused hyperlipidemia, depletion of adipose tissue, a slight increase of heart lipid content, lipid accretion in the tumor cells and a relative increase of free fatty acids and cholesterol in the ascites fluid. LPLA of the post-heparin plasma was higher in tumorous than in control mice. Tumor growth led to a marked decline of LPLA in the adipose tissue and an elevation in the heart. It declined slightly in the older tumor cells and increased in the ascites plasma of the same. It has been concluded that: a) decline in adipose tissue LPLA may play an important part in the development of hyperlipidemia and loss of body fat; b) increase of the heart LPLA proves insufficient for elimination of the piled up blood lipids during progression; c) LPLA in the ascites fluid may favour the hydrolysis of triglycerides entering the ascites fluid, which might account at least in part for the fatty acids made available to the tumor; d) LPLA detected in the tumor cells might also facilitate the assimilation of lipids by the tumor cells.

摘要

对携带艾氏腹水瘤的小鼠血清及各种组织的脂质含量和脂蛋白脂肪酶活性(LPLA)进行了研究。生长中的肿瘤导致高脂血症、脂肪组织消耗、心脏脂质含量略有增加、肿瘤细胞脂质蓄积以及腹水中游离脂肪酸和胆固醇相对增加。荷瘤小鼠肝素后血浆的LPLA高于对照小鼠。肿瘤生长导致脂肪组织中LPLA显著下降,心脏中LPLA升高。在较老的肿瘤细胞中LPLA略有下降,而在相同肿瘤的腹水血浆中则升高。得出以下结论:a)脂肪组织LPLA下降可能在高脂血症和体脂丢失的发展中起重要作用;b)心脏LPLA增加证明在疾病进展过程中不足以消除堆积的血脂;c)腹水中的LPLA可能有利于进入腹水的甘油三酯的水解,这可能至少部分解释了肿瘤可利用的脂肪酸来源;d)在肿瘤细胞中检测到 的LPLA也可能促进肿瘤细胞对脂质的同化。

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Existence of lipoprotein lipase in human sarcomas and carcinomas.人肉瘤和癌中脂蛋白脂肪酶的存在。
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