Ikeda T, Nishikawa A, Imazawa T, Kimura S, Hirose M
Division of Pathology, National Institute of Health Sciences,1-18-1 Kamiyoga, Setagaya-ku, Tokyo 158-8501, Japan.
Carcinogenesis. 2000 Apr;21(4):707-13. doi: 10.1093/carcin/21.4.707.
The effects of defatted soybean and/or iodine-deficient diet feeding were investigated in female F344 rats. Rats were divided into four groups, each consisting of 10 animals, and fed basal AIN-93G diet in which the protein was exchanged for 20% gluten (Group 1), iodine-deficient gluten (Group 2), 20% defatted soybean (Group 3) and iodine-deficient defatted soybean (Group 4). At week 10, relative thyroid gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 2 (15.5 +/- 1.3) and 4 (81.7 +/- 8.6) than in Group 1 (8.4 +/- 2.0) and pituitary gland weights (mg/100 g body wt) were significantly (P < 0.01) higher in Groups 3 (9.1 +/- 0. 6) and 4 (9.7 +/- 1.5) than in Group 1 (6.5 +/- 1.5). Serum biochemical assays revealed thyroxine to be significantly (P < 0.05) lower in Groups 2 and 4 than in Group 1. On the other hand, serum thyroid-stimulating hormone (TSH) was significantly (P < 0.01) higher in Groups 3 and 4 than in Group 1. This was particularly striking for TSH (ng/ml) at week 10 in Group 4 (126 +/- 11) as compared with Groups 1 (4.36 +/- 0.30), 2 (4.84 +/- 0.80) and 3 (5. 78 +/- 0.80). Histologically, marked diffuse follicular hyperplasia of the thyroid was evident in Group 4 rats. Proliferating cell nuclear antigen labeling indices (%) were significantly higher (P < 0.05) in Groups 2 (4.8 +/- 2.5) and 4 (13.2 +/- 1.1) than in Group 1 (0.4 +/- 0.5). Ultrastructurally, severe disorganization and disarrangement of mitochondria were apparent in thyroid follicular cells of Group 4. In the anterior pituitary, dilated rough surfaced endoplasmic reticulum and increased secretory granules were remarkable in this group. Our results thus strongly suggest that dietary defatted soybean synergistically stimulates the growth of rat thyroid with iodine deficiency, partly through a pituitary-dependent pathway.
在雌性F344大鼠中研究了脱脂大豆和/或缺碘饮食喂养的影响。大鼠被分为四组，每组10只动物，分别喂食基础AIN - 93G饮食，其中蛋白质被20%的谷蛋白替代（第1组）、缺碘谷蛋白（第2组）、20%脱脂大豆（第3组）和缺碘脱脂大豆（第4组）。在第10周时，第2组（15.5±1.3）和第4组（81.7±8.6）的相对甲状腺重量（mg/100 g体重）显著高于第1组（8.4±2.0）（P<0.01），第3组（9.1±0.6）和第4组（9.7±1.5）的垂体重量（mg/100 g体重）显著高于第1组（6.5±1.5）（P<0.01）。血清生化检测显示，第2组和第4组的甲状腺素显著低于第1组（P<0.05）。另一方面，第3组和第4组的血清促甲状腺激素（TSH）显著高于第1组（P<0.01）。与第1组（4.36±0.30）、第2组（4.84±0.80）和第3组（5.78±0.80）相比，第4组在第10周时的TSH（ng/ml）尤其显著升高（126±11）。组织学上，第4组大鼠甲状腺明显出现显著的弥漫性滤泡增生。第2组（4.8±2.5）和第4组（13.2±1.1）的增殖细胞核抗原标记指数（%）显著高于第1组（0.4±0.5）（P<0.05）。超微结构上，第4组甲状腺滤泡细胞中线粒体严重紊乱和排列失调。在垂体前叶，该组中扩张的粗面内质网和增加的分泌颗粒很明显。因此，我们的结果强烈表明，饮食中的脱脂大豆与碘缺乏协同刺激大鼠甲状腺生长，部分通过垂体依赖途径。
