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链脲佐菌素诱导的糖尿病大鼠睾丸间质细胞的超微结构变化

Ultrastructural changes in Leydig cells of streptozotocin-induced diabetic rats.

作者信息

Orth J M, Murray F T, Bardin C W

出版信息

Anat Rec. 1979 Nov;195(3):415-30. doi: 10.1002/ar.1091950302.

Abstract

Hyperglycemia (experimental diabetes) was induced in adult male rats by destruction of the pancreatic beta cells with a single intravenous injection of streptozotocin (STZ). Testes from diabetic, from insulin-treated diabetic, and from sham-injected normal rats were fxed by vascular perfusion. The fine structure of Leydig cells was examined at two, three, and four weeks after the STZ injection in the untreated diabetic animals, and at four weeks in the controls and insulin-treated diabetic rats. A number of morphological changes was observed in Leydig cells of untreated diabetic animals. Most obvious of these was an accumulation of lipid droplets, not normally present in Leydig cells in adults of this species. Smooth endoplasmic reticulum (SER) was markedly reduced in Leydig cells of the hyperglycemic rats. Several types of intracellular bodies were seen exclusively in Leydig cells of the untreated diabetic animals. Many resembled secondary lysosomes or dense bodies, while others appeared to be autophagic vacuoles. In addition, a small, granule-containing lamellar structure was seen either within a typical dense body or free in the cytoplasm. Myelin-like structures were commonly observed within the cytoplasm of the Leydig cell or within mitochondria. The appearance of the mitochondria in diabetic rats was otherwise normal. The extracellular spaces surrounding Leydig cells from untreated hyperglycemic rats also contained large accumulations of myelin-like material. These structural changes appear to be direct consequences of the diabetic state of the animals, since the ultrastructure of insulin-treated diabetic rats did not differ from that of the controls. These findings may reflect an alteration or breakdown of Leydig cell components normally involved in the synthesis of androgen, and correlate with previous reports of lowered circulating levels of testosterone in diabetic rats.

摘要

通过单次静脉注射链脲佐菌素(STZ)破坏成年雄性大鼠的胰腺β细胞来诱导高血糖症(实验性糖尿病)。对糖尿病大鼠、胰岛素治疗的糖尿病大鼠以及假注射的正常大鼠的睾丸进行血管灌注固定。在未治疗的糖尿病动物中,于注射STZ后的两周、三周和四周检查睾丸间质细胞的精细结构,并在对照组和胰岛素治疗的糖尿病大鼠中于四周时进行检查。在未治疗的糖尿病动物的睾丸间质细胞中观察到了许多形态学变化。其中最明显的是脂滴的积累,而在该物种的成年动物的睾丸间质细胞中通常不存在这种情况。高血糖大鼠的睾丸间质细胞中滑面内质网(SER)明显减少。在未治疗的糖尿病动物的睾丸间质细胞中仅可见几种类型的细胞内小体。许多类似次级溶酶体或致密体,而其他的似乎是自噬泡。此外,在典型的致密体内或细胞质中可看到一种小的、含颗粒的层状结构。在睾丸间质细胞的细胞质内或线粒体内通常可观察到髓鞘样结构。糖尿病大鼠的线粒体外观在其他方面是正常的。来自未治疗的高血糖大鼠的睾丸间质细胞周围的细胞外空间也含有大量髓鞘样物质的积累。这些结构变化似乎是动物糖尿病状态的直接后果,因为胰岛素治疗的糖尿病大鼠的超微结构与对照组没有差异。这些发现可能反映了通常参与雄激素合成的睾丸间质细胞成分的改变或破坏,并与先前关于糖尿病大鼠循环睾酮水平降低的报道相关。

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