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地塞米松处理大鼠中产生葡萄糖依赖性促胰岛素多肽的K细胞

Glucose-dependent insulinotropic polypeptide-producing K cells in dexamethasone-treated rats.

作者信息

Koko V, Glisic R, Todorovic V, Drndarevic N, Mitrovic O

机构信息

University of Belgrade, Institute for Medical Research, Belgrade.

出版信息

J Microsc. 2008 Dec;232(3):493-7. doi: 10.1111/j.1365-2818.2008.02146.x.

DOI:10.1111/j.1365-2818.2008.02146.x
PMID:19094027
Abstract

Some studies indicate that diabetes mellitus exerts an influence on the gastrointestinal tract and its diffuse neuroendocrine system (DNES) in regard to cellular density and neuroendocrine content. Since there is no data about relationship between experimentally induced non-insulin-dependent (type 2) diabetes mellitus (NIDDM) on the gut K cells, the aim of our study was to investigate immunohistochemical, stereological and ultrastructural changes of rat K cells after 12 days of dexamethasone treatment. Twenty male Wistar rats aged 30 days were given daily intraperitoneally 2 mg kg(-1) dexamethasone (group DEX, 10 rats) or saline (group C, 10 rats) for 12 days. Tissue specimens were obtained from each antrum with corpus and different parts of the small (SI) and large intestine (LI) of all animals. Immunohistochemistry was carried out using antisera against the GIP and insulin. Transmission electron microscopy was also used. Although, according to the literature data, rat K cells are present in the duodenum and jejunum and, to a lesser extent, in the ileum, in the present study we observed that those cells were abundant also in all parts of the LI. We observed generally that GIP-producing K cells were augmented in all parts of SI and decreased in the LI of DEX rats. Insulin immunoreactivity (ir) coexpressed with GIP-ir in K cells and was stronger in the SI of DEX rats as compared with C rats. We also found by electron microscopy that small intestinal K cells have features not only of GIP-secreted but also of insulin-secreted cells. We concluded that dexamethasone treatment caused proliferation of K cells in the rat SI, and simultaneously transformation of GIP-producing K cells to insulin-synthesizing cells.

摘要

一些研究表明,糖尿病会对胃肠道及其弥散神经内分泌系统(DNES)的细胞密度和神经内分泌含量产生影响。由于尚无关于实验性诱导的非胰岛素依赖型(2型)糖尿病(NIDDM)与肠道K细胞之间关系的数据,我们研究的目的是调查地塞米松治疗12天后大鼠K细胞的免疫组织化学、体视学和超微结构变化。将20只30日龄雄性Wistar大鼠每天腹腔注射2 mg kg(-1)地塞米松(DEX组,10只大鼠)或生理盐水(C组,10只大鼠),持续12天。从所有动物的胃窦、胃体以及小肠(SI)和大肠(LI)的不同部位获取组织标本。使用抗GIP和胰岛素的抗血清进行免疫组织化学检测。同时也使用了透射电子显微镜。尽管根据文献数据,大鼠K细胞存在于十二指肠和空肠,在回肠中数量较少,但在本研究中我们观察到这些细胞在大肠的所有部位也很丰富。我们普遍观察到,产生GIP的K细胞在DEX大鼠的小肠各部位增加,在大肠中减少。与C组大鼠相比,K细胞中与GIP-ir共表达的胰岛素免疫反应性(ir)在DEX大鼠的小肠中更强。我们还通过电子显微镜发现,小肠K细胞不仅具有分泌GIP的细胞特征,还具有分泌胰岛素的细胞特征。我们得出结论,地塞米松治疗导致大鼠小肠中K细胞增殖,同时使产生GIP的K细胞转变为合成胰岛素的细胞。

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