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在Goto-Kakizaki糖尿病大鼠腮腺中,腺泡细胞的葡萄糖转运蛋白1(GLUT1)表达增加并定位于高尔基体。

Increased GLUT1 expression and localization to Golgi apparatus of acinar cells in the parotid gland of Goto-Kakizaki diabetic rats.

作者信息

Maruo Kohki, Nishiyama Megumi, Honda Yuko, Cao Ai-Lin, Gao Wei-Qi, Shibata Kentaro, Murata Yuzo, Kido Mizuho A

机构信息

Department of Anatomy and Physiology, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan.

Department of Pathology and Microbiology, Faculty of Medicine, Saga University, 5-1-1 Nabeshima, Saga 849-8501, Japan.

出版信息

Arch Oral Biol. 2023 Feb;146:105601. doi: 10.1016/j.archoralbio.2022.105601. Epub 2022 Dec 5.

Abstract

OBJECTIVE

Patients with diabetes are known to have high salivary glucose levels. But the mechanisms are still unclear. We hypothesized that the topological changes of glucose transporters affect the salivary glucose level.

METHODS

We used adult Goto-Kakizaki (GK) rats, an animal model of advanced diabetes, and Wistar rats as a control, with or without glucose load. The sections of salivary glands from the animals were processed for standard histological, immunohistochemical, and immunofluorescent staining.

RESULTS

Parotid acinar cells of GK rats appeared like mucous filled with low-eosin-stained granules and possessing a flat nucleus located basally, whereas those of Wistar rats appeared as a typical serous gland with eosin-rich cytoplasm and a spherical nucleus. Cytoplasmic granules of GK rat parotid acinar cells showed no reaction of polysaccharide staining. In acinar cell cytoplasm of GK rats, intense GLUT1 immunoreactivity was observed compared to Wistar rats. By double immunostaining for GLUT1 and Golgi apparatus-specific markers, it was determined that GLUT1 was localized to the Golgi apparatus. By glucose loading in starved GK rats, the distribution of GLUT1-immunoreactive signals was spread out clearly from the apical side of the nucleus to the basolateral side.

CONCLUSIONS

In rat model of diabetes, highly localized GLUT1 at Golgi apparatus in acinar cells seems to increase taking up cytoplasmic glucose to form exocytotic vesicles. This phenomenon may transform parotid glands from serous to mucous-like and result in saccharide-rich saliva.

摘要

目的

已知糖尿病患者唾液葡萄糖水平较高。但其机制仍不清楚。我们推测葡萄糖转运体的拓扑变化会影响唾液葡萄糖水平。

方法

我们使用成年Goto-Kakizaki(GK)大鼠(一种晚期糖尿病动物模型)和Wistar大鼠作为对照,给予或不给予葡萄糖负荷。对动物的唾液腺切片进行标准组织学、免疫组织化学和免疫荧光染色处理。

结果

GK大鼠的腮腺腺泡细胞看起来像充满黏液的细胞,含有低嗜酸性染色颗粒,细胞核位于基部且扁平,而Wistar大鼠的腮腺腺泡细胞则表现为典型的浆液性腺,细胞质富含嗜酸性物质,细胞核呈球形。GK大鼠腮腺腺泡细胞的细胞质颗粒未显示多糖染色反应。与Wistar大鼠相比,在GK大鼠的腺泡细胞质中观察到强烈的GLUT1免疫反应性。通过对GLUT1和高尔基体特异性标志物进行双重免疫染色,确定GLUT1定位于高尔基体。通过对饥饿的GK大鼠给予葡萄糖负荷,GLUT1免疫反应性信号的分布从细胞核的顶端侧清晰地扩展到基底外侧侧。

结论

在糖尿病大鼠模型中,腺泡细胞高尔基体上高度定位的GLUT1似乎会增加对细胞质葡萄糖的摄取以形成胞吐小泡。这种现象可能会使腮腺从浆液性转变为黏液样,并导致唾液富含糖类。

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