Lhuillery C, Bougnoux P, Groscolas R, Durand G
Laboratoire de Nutrition et Sécurité Alimentaire, Institut National de la Recherche Agronomique, Jouy en Josas, France.
Nutr Cancer. 1995;24(3):299-309. doi: 10.1080/01635589509514419.
Previous work in breast cancer patients has indicated an inverse relationship between the risk of relapse and the alpha-linolenic acid (18:3n-3) level in adipose breast tissue. To determine whether low alpha-linolenic levels in patients with aggressive breast cancer resulted from lower 18:3n-3 dietary intake and/or increased metabolism of stored 18:3n-3, we analyzed the fatty acid composition of mammary adipose tissue during tumor growth in a rat model of mammary carcinogenesis. Rats were fed a diet containing 10% fat as rapeseed oil (in which 9% of total fatty acids is 18:3n-3). one-half of the rats received an injection of nitrosomethylurea (NMU) to initiate mammary tumors. In control and NMU-treated groups, three to five animals were sacrificed every three weeks during the five-month experimental time. tumor growth was followed by weekly palpation of the animals and by the measure of total tumor mass and number in sacrificed rats. Mammary tumor and adipose tissues were sampled in sacrificed rats. We found that although mammary adipose tissue fatty acid profile changed throughout the experiment, there was no difference in fatty acid profile between control and NMU-treated rats of the same age. In the NMU-treated group, 18:3n-3 level remained identical throughout the experimental period, irrespective of tumor burden. These data show that, in this model, mammary tumor growth does not modify stored fatty acid levels, including 18:3n-3. this suggests that decreased 18:3n-3 level in patients with poor prognosis is not a consequence of tumor burden but more likely depends on decreased dietary intake.
先前针对乳腺癌患者的研究表明,乳腺脂肪组织中复发风险与α-亚麻酸(18:3n-3)水平呈负相关。为了确定侵袭性乳腺癌患者体内α-亚麻酸水平较低是由于18:3n-3膳食摄入量较低和/或储存的18:3n-3代谢增加所致,我们在乳腺癌发生的大鼠模型中分析了肿瘤生长过程中乳腺脂肪组织的脂肪酸组成。给大鼠喂食含10%脂肪的菜籽油(其中9%的总脂肪酸为18:3n-3)。一半的大鼠注射亚硝基甲基脲(NMU)以引发乳腺肿瘤。在对照和NMU处理组中,在为期五个月的实验期间,每三周处死三到五只动物。通过每周触诊动物以及测量处死大鼠的肿瘤总质量和数量来跟踪肿瘤生长。在处死的大鼠中采集乳腺肿瘤和脂肪组织样本。我们发现,尽管在整个实验过程中乳腺脂肪组织的脂肪酸谱发生了变化,但相同年龄的对照大鼠和NMU处理大鼠的脂肪酸谱没有差异。在NMU处理组中,无论肿瘤负荷如何,18:3n-3水平在整个实验期间都保持不变。这些数据表明,在该模型中,乳腺肿瘤生长不会改变储存的脂肪酸水平,包括18:3n-3。这表明预后不良患者体内18:3n-3水平降低不是肿瘤负荷的结果,而更可能取决于膳食摄入量的减少。