Morphological and histopathological changes in tongues of experimentally developed acromegaly-like rats

Morphological and histopathological changes in tongues of experimentally developed acromegaly-like rats
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DOI:
10.1055/s-2006-925176
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发表时间:
2006-03-01
影响因子:
2.2
通讯作者:
Sasano, T.
Sasano, T.
中科院分区:
医学4区
文献类型:
--
作者:
Kobayashi, A.;Iikubo, M.;Sasano, T.

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最近开发的一种肢端肥大症样大鼠模型,外源性胰岛素样生长因子I(IGF-I)的管理,用于调查形态和组织病理学的舌变化,并澄清这些变化是否是可逆的。将人重组IGF-I(640 μ g/天)连续皮下输注到10周龄的雄性大鼠中4周(IGF-I组; n=6)。对照假手术动物仅注射生理盐水(对照组; n=6)。在14周龄结束给药时立即处死大鼠。另外12只大鼠(每组6只)在给药结束后再圈养4周。总IGF-I(人+大鼠)在给药期间显著增加,之后恢复至对照水平。与对照组大鼠相比,IGF-I组中存在组织病理学变化(肌束宽度、肌束之间的空间和上皮厚度增加),舌重量显著增加。停止IGF-I给药后,舌大小恢复至对照水平。这些研究结果表明,在我们的肢端肥大症样大鼠模型中实验性开发了特征性舌增大,并且这种形态学和组织病理学舌变化在循环IGF-I水平正常化时是可逆的。
An acromegaly-like rat model recently developed by exogenous administration of insulin-like growth factor I (IGF-I) was used to investigate morphological and histopathological tongue changes and clarify whether the changes were reversible. Human recombinant IGF-I (640 mu g/day) was-continuously subcutaneously infused into ten-week-old male rats for four weeks (IGF-I group; n=6). Control sham-operated animals were injected saline alone (control group; n=6). Rats were sacrificed immediately on ending administration at the age of fourteen weeks. Another 12 rats (6 from each group) were housed for an additional four weeks after administration ended. Total IGF-I (human + rat) increased significantly during administration, returning to control levels afterwards. Tongue weights significantly increased with histopathological changes present (increases in the muscle-bundle width, spaces between muscle-bundles and epithelium thickness) in the IGF-I group compared to control rats. Tongue size returned to control levels after discontinuation of IGF-I administration. These findings suggest that the characteristic tongue enlargement was developed experimentally in our acromegaly-like rat model, and that such morphological and histopathological tongue changes are reversible on normalization of circulating IGF-I levels.