Westin T, Zachrisson H, Edström S, Lundholm K
Department of Otolaryngology and Surgery, University of Gothenburg, Sahlgrenska Hospital, Sweden.
Eur J Cancer. 1991;27(10):1282-8. doi: 10.1016/0277-5379(91)90098-x.
Ornithine decarboxylase (ODC) and S-adenosylmethionine decarboxylase activity (SAMD) were measured in tumour tissue in mice during periods of starvation (24 h) and refeeding. Starvation led to a 60% reduction in tumour ODC activity. Refeeding normalised the activity within 4 h. Restitution in ODC activity, representing de novo enzyme synthesis, preceded DNA resynthesis. SAMD activity continued to fall along the increase in ODC activity during refeeding, while difluoro-methyl-ornithine (DFMO) caused a compensatory increase in SAMD activity as expected. A fall and regain in ODC activity was associated with inhibition and regrowth of the tumour. Starvation-refeeding was not related to any decrease in tumour polyamine concentrations, while systemic DFMO blockade was. Glucose stimulated ODC when refed orally, but not when given systemically. Tumour ODC activity was not decreased in refed mice by anti-insulin, a procedure that antagonised insulin's bioactivity. Exogenous insulin did not stimulate tumour ODC activity. Our results suggest that gastrointestinal metabolism of carbohydrates stimulates the release of a factor, which initiates both ODC activity and DNA synthesis in tumour cells. This factor was not insulin.
在小鼠饥饿（24小时）和再喂食期间，测定肿瘤组织中的鸟氨酸脱羧酶（ODC）和S-腺苷甲硫氨酸脱羧酶活性（SAMD）。饥饿导致肿瘤ODC活性降低60%。再喂食4小时内活性恢复正常。ODC活性的恢复，代表从头合成酶，先于DNA再合成。再喂食期间，随着ODC活性增加，SAMD活性持续下降，而二氟甲基鸟氨酸（DFMO）如预期引起SAMD活性代偿性增加。ODC活性的下降和恢复与肿瘤的抑制和再生长相关。饥饿-再喂食与肿瘤多胺浓度的任何降低无关，而全身性DFMO阻断则有关。口服葡萄糖再喂食时刺激ODC，但全身给药时则不然。抗胰岛素可拮抗胰岛素的生物活性，但再喂食小鼠的肿瘤ODC活性并未降低。外源性胰岛素不刺激肿瘤ODC活性。我们的结果表明，碳水化合物的胃肠代谢刺激一种因子的释放，该因子启动肿瘤细胞中的ODC活性和DNA合成。该因子不是胰岛素。
