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作为导致携带包皮腺肿瘤ESR - 586的C57BL小鼠脂质消耗的因素,修饰的脂蛋白脂肪酶活性、脂肪生成速率和脂肪分解速率。

Modified lipoprotein lipase activities, rates of lipogenesis, and lipolysis as factors leading to lipid depletion in C57BL mice bearing the preputial gland tumor, ESR-586.

作者信息

Thompson M P, Koons J E, Tan E T, Grigor M R

出版信息

Cancer Res. 1981 Aug;41(8):3228-32.

PMID:7248977
Abstract

The biochemical basis for the observed depletion of adipose tissue in C57BL mice bearing a transplantable nonmetastasizing preputial gland tumor, ESR-586, has been investigated. The results have shown that there are a number of significant changes in both deposition and mobilization of lipid as the tumor grows. The first change, before the tumor reached 2 g, was a decline in the activity of adipose tissue lipoprotein lipase to levels normally found in starved animals. This was accompanied by a slight increase in lipoprotein lipase activity in heart and appearance of substantial activity in large tumors. Together, these would result in impaired uptake of exogenous fatty acids by adipose tissue, and dietary lipid would be directed away from storage. This was followed by a marked decline in endogenous lipid synthesis in adipose tissue which commenced when the tumor weighed between 2 and 3 g, as measured in vivo by the incorporation of radioactivity into lipid from tritiated water. The basal rate of lipolysis was enhanced 2-fold in epididymal fat pads from mice bearing tumors that weighed between 2 and 4 g, although there was no difference in the epinephrine-stimulated activity.

摘要

对携带可移植性非转移性包皮腺肿瘤ESR - 586的C57BL小鼠脂肪组织消耗现象的生化基础进行了研究。结果表明,随着肿瘤生长,脂质的沉积和动员发生了许多显著变化。第一个变化发生在肿瘤重量达到2 g之前,即脂肪组织脂蛋白脂肪酶活性下降至饥饿动物通常所见的水平。与此同时,心脏中脂蛋白脂肪酶活性略有增加,并且在大肿瘤中出现了大量活性。这些变化共同导致脂肪组织对外源性脂肪酸摄取受损,膳食脂质将不再用于储存。接下来,当肿瘤重量在2至3 g之间时,脂肪组织内源性脂质合成显著下降,这是通过在体内测量氚标记水的脂质放射性掺入来确定的。在肿瘤重量为2至4 g的小鼠附睾脂肪垫中,基础脂肪分解率提高了2倍,尽管肾上腺素刺激的活性没有差异。

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