López-Soriano J, Argilés J M, López-Soriano F J
Departament de Bioquímica i Biologia Molecular, Facultat de Biologia, Universitat de Barcelona, Spain.
Cancer Lett. 1997 Jun 24;116(2):159-65. doi: 10.1016/s0304-3835(97)00173-0.
The implantation of the Yoshida AH-130 ascites hepatoma to rats resulted in an exponential growth of the tumour cells followed by a late stationary phase. The tumour burden was accompanied by a dramatic decrease in body weight. Tumour growth was associated with a marked hypertriglyceridaemia during the period of exponential growth, while in the stationary phase the plasma triacylglycerol concentration was similar to that observed in the non-tumour-bearing animals. Similar increases were observed, following tumour inoculation, in the plasma concentrations of non-esterified fatty acids and glycerol, suggesting an intense lipolytic activity. These changes in lipaemia were associated with a marked decrease in LPL activity in white adipose tissue; in contrast, LPL activity was increased in the tumour-bearing animals in brown adipose tissue at day 6 following inoculation and in the heart during most of the period studied. Although the presence of the tumour did not induce any changes in blood lactate concentrations, it caused a decrease in circulating glucose; conversely, the tumour induced an important increase in the concentration of circulating ketone bodies, suggesting a metabolic adaptation of the tumour-bearing rats to glucose sparing and alternative fuel utilization. It may be suggested that the hyperlipidaemia present in the Yoshida AH-130 bearing rats is partly due to a decreased LPL activity in white adipose tissue which does not seem to be influenced by changes in insulin circulating concentrations.
将吉田AH - 130腹水肝癌移植到大鼠体内会导致肿瘤细胞呈指数增长,随后进入晚期静止期。肿瘤负荷伴随着体重的显著下降。在指数增长期,肿瘤生长与明显的高甘油三酯血症相关,而在静止期,血浆甘油三酯浓度与未荷瘤动物相似。接种肿瘤后,血浆中非酯化脂肪酸和甘油的浓度也有类似升高,表明存在强烈的脂解活性。这些血脂变化与白色脂肪组织中脂蛋白脂肪酶(LPL)活性的显著降低有关;相反,接种后第6天,荷瘤动物棕色脂肪组织中的LPL活性增加,且在研究的大部分时间内心脏中的LPL活性也增加。虽然肿瘤的存在并未引起血乳酸浓度的任何变化,但它导致循环葡萄糖水平降低;相反,肿瘤导致循环酮体浓度显著升高,这表明荷瘤大鼠在代谢上适应了葡萄糖节约和替代燃料利用。可以推测,吉田AH - 130荷瘤大鼠出现的高脂血症部分是由于白色脂肪组织中LPL活性降低,而这似乎不受循环胰岛素浓度变化的影响。