糖尿病大鼠胰腺的形态功能状态

O. Ivantsiv, V. Fedorak, I. Bilinskyi, Yu.I. Popovych, V.V. Fedorak
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引用次数: 0

摘要

目的分析有关白实验鼠糖尿病和治疗时胰腺形态功能状态的文献资料。材料和方法。归纳乌克兰和外国文献数据、荟萃分析结果和随机研究结果。结果。在实验动物中建立糖尿病模型的主要机制特点。有关胰岛在正常情况下、糖尿病情况下和药物治疗糖尿病情况下的特殊性的文献资料得到了加强。在解剖学上,胰腺分为三个区域:十二指肠、胃和脾。由于大鼠的器官较小,这种划分在一定程度上是有条件的。在某些情况下,脾脏区域的内分泌胰岛浓度最高。胰岛由内分泌细胞形成。大鼠体内有四种内分泌细胞:胰岛素细胞、胰高血糖素细胞、体节细胞和胰多肽细胞。糖尿病大鼠的胰腺形态功能状态恶化。胰岛细胞数量和胰岛面积减少,葡萄糖和糖化血红蛋白水平升高。文献资料显示,实验性糖尿病会给实验动物带来不适,降低实验动物的质量和寿命,因此这项研究具有重要的社会意义。长期未纠正的高血糖为微血管病和大血管病的发生提供了背景。糖尿病药物疗法的主要目的是通过饮食纠正并结合药物治疗达到血糖正常。这不仅能减缓糖尿病微血管病和大血管病变的发展,还能延长大鼠的寿命。在胰岛素绝对缺乏的情况下,纠正链脲佐菌素诱发糖尿病的当务之急仍然是使用外源性胰岛素药物进行胰岛素治疗,并通过改善内分泌细胞的再生来加强腺体的修复过程。科学家的首要任务仍然是开发能够促进胰岛再生过程的药物。据文献资料显示,与单一疗法相比,使用药物抗糖尿病疗法对糖尿病进行综合治疗更为有效。一些学者研究了胰岛素和艾塞那肽(一种增量素模拟物)的联合作用,发现艾塞那肽能增强糖尿病患者胰岛的再生能力。然而,增量肽模拟物在Ⅰ型糖尿病中的应用仍存在争议,需要进一步研究。糖尿病实验模型的可行性在于开发新的Ⅰ型糖尿病矫治方法。这将延长内分泌细胞的功能,加强胰腺的再生和代偿过程,优化实验中抗糖尿病药物的治疗效果。结论所提供的数据确定了糖尿病发病机制中胰岛形态变化的特殊性,证实了在营养和治疗的帮助下,通过使碳水化合物代谢正常化、激活胰岛的代偿-恢复过程和再生,对链脲佐菌素诱导的实验动物糖尿病进行药物治疗的必要性。综合疗法和营养正常化可减缓糖尿病微血管病变和大血管病变以及糖尿病心血管事件的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MORPHOFUNCTIONAL STATE OF PANCREAS IN RATS WITH DIABETES MELLITUS
Goal. To analyze the literature sources concerning morphofunctional state of a pancreas in case of diabetes mellitus and treatment in white laboratory rats. Materials and methods. Generalisation of ukrainian and foreign literature data, results of meta-analyses and randomized studies. Results. Characteristics of main mechanisms of diabetes mellitus modeling was conducted in experimental animals. Literature data regarding the peculiarities of pancreatic islets in normal conditions, in case of diabetes mellitus and pharmacological correction of this disease were intensified. Anatomically, pancreas is divided into three regions: duodenal, gastric and splenic. This division in rats is somewhat conditional due to small size of organ. In some cases, highest concentration of endocrine islets is found in splenic region of gland. Islets are formed by endocrinocytes. There are four types of endocrine cells in rats: insulinocytes, glucagonocytes, somatostatinocytes and pancreatic polypeptide cells. In rats with diabetes, morphofunctional state of pancreas worsens. Numbers of insulinocytes and area of ​​islets are decreases, level of glucose and glycosylated hemoglobin increases. Review of literature sources shows social significance of conducted research, as experimental diabetes mellitus creates discomfort and reduces the quality and lifespan of experimental animals. Prolonged uncorrected hyperglycemia creates the background for micro- and macroangiopathies development. Pharmacotherapy for diabetes primarily aims to achieve normoglycemia through dietary correction in combination with pharmacological agents. This not only slows down the progression of diabetic micro- and macroangiopathies but also extends the lives of rats. In context of absolute insulin deficiency, a priority for correcting streptozotocin-induced diabetes remains using of insulin therapy with exogenous insulin drugs and enhancing reparative processes in the gland due to improved regeneration of endocrinocytes. The priority task for scientists still remains the development of medicines capable of promoting regeneration processes of islets. According to literature sources, polytherapy of diabetes mellitus using pharmacological antidiabetic drugs can be more effective as compared to monotherapy. Several authors have studied the combined effect of insulin and exenatide (an incretin mimetic), finding that exenatide enhances the regenerative capabilities of pancreatic islets in diabetes mellitus. However, the use of incretin mimetics in type І diabetes mellitus remains controversial and requires further study. Expediency of experimental diabetes mellitus modeling is based on developing new methods for type І diabetes mellitus correction. This will promote prolonged functioning of endocrine cells, enhance regeneratory and compensatory processes in pancreas and optimize the therapeutic effect of antidiabetic drugs in experiment. Conclusion. The presented data establish the peculiarities of morphological changes in pancreatic islets in pathogenesis of diabetes, confirm the necessity of pharmacological correction of streptozotocine-induced diabetes in experimental animals by normalizing carbohydrate metabolism, activating compensatory-recovery processes and regenerations of islets with the help of nutrition and treatment. Comprehensive polytherapy and normalization of nutrition allow for the slowing of the development of diabetic micro- and macroangiopathies and cardiovascular events in the context of diabetes.
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