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肥胖糖尿病小鼠(人类2型糖尿病动物模型)的肠肌丛

Myenteric plexus of obese diabetic mice (an animal model of human type 2 diabetes).

作者信息

Spångéus A, El-Salhy M

机构信息

Department of Medicine, University Hospital, Umeå, Sweden.

出版信息

Histol Histopathol. 2001 Jan;16(1):159-65. doi: 10.14670/HH-16.159.

Abstract

The myenteric plexus of the gastrointestinal tract was investigated in the obese diabetic mouse, an animal model of human type 2 diabetes. Sections were immunostained by the avidin-biotin complex method, using a general nerve marker, protein gene product 9.5 (PGP 9.5), as well as antibodies to several important neurotransmitters. Computerized image analysis was used for quantification. When diabetic mice were compared with controls, no difference was found in the density of PGP 9.5-immunoreactive (IR) nerve fibres in antrum, duodenum or colon. In antrum and duodenum, diabetic mice showed a decreased number of vasoactive intestinal peptide (VIP)-IR neurons in myenteric ganglia as well a decreased relative volume density in myenteric plexus (though not significantly in antrum, p=0.073). No difference was found regarding VIP-IR nerves in colon. The volume density of nitric oxide synthase (NOS)-IR nerve fibres was decreased in antrum and duodenum of diabetic mice, whereas no difference was found in colon. The density of galanin-IR nerve fibres was decreased in duodenum. Whereas neuropeptide Y (NPY)- and vesicular acetylcholine transporter (VAChT)-IR nerve fibres was increased in density in colon of diabetic mice, no difference was found in antrum and duodenum. Regarding substance P, there was no difference between diabetic and control mice in antrum, duodenum or colon. The present study shows that gut innervation is affected in this animal model of human type 2 diabetes. It is possible that the present findings may have some relevance for the gastrointestinal dysfunctions seen in patients with type 2 diabetes.

摘要

在肥胖糖尿病小鼠(一种人类2型糖尿病动物模型)中,对胃肠道的肌间神经丛进行了研究。切片采用抗生物素蛋白-生物素复合物法进行免疫染色,使用一种通用神经标志物蛋白基因产物9.5(PGP 9.5)以及针对几种重要神经递质的抗体。采用计算机图像分析进行定量分析。将糖尿病小鼠与对照小鼠相比,胃窦、十二指肠或结肠中PGP 9.5免疫反应性(IR)神经纤维的密度未发现差异。在胃窦和十二指肠中,糖尿病小鼠肌间神经节中血管活性肠肽(VIP)-IR神经元数量减少,肌间神经丛的相对体积密度也降低(尽管在胃窦中差异不显著,p = 0.073)。结肠中VIP-IR神经未发现差异。糖尿病小鼠胃窦和十二指肠中一氧化氮合酶(NOS)-IR神经纤维的体积密度降低,而结肠中未发现差异。十二指肠中甘丙肽-IR神经纤维的密度降低。糖尿病小鼠结肠中神经肽Y(NPY)和囊泡乙酰胆碱转运体(VAChT)-IR神经纤维的密度增加,而胃窦和十二指肠中未发现差异。关于P物质,糖尿病小鼠与对照小鼠在胃窦、十二指肠或结肠中没有差异。本研究表明,在这种人类2型糖尿病动物模型中,肠道神经支配受到影响。目前的研究结果可能与2型糖尿病患者出现的胃肠功能障碍有一定关联。

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