INDUCTION OF DIABETES BY STREPTOZOTOCIN IN RATS

INDUCTION OF DIABETES BY STREPTOZOTOCIN IN RATS
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DOI:
10.1007/bf02913315
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发表时间:
2007-09-01
影响因子:
2.1
通讯作者:
Rad, B. Lame
Rad, B. Lame
中科院分区:
其他
文献类型:
--
作者:
Akbarzadeh, A.;Norouzian, D.;Rad, B. Lame

文献摘要

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本研究用链脲佐菌素(Streptozotocin,STZ)诱发正常成年Wistar大鼠实验性糖尿病,比较正常和糖尿病大鼠的体重、饮水量、饮水量、尿量、血糖、胰岛素和C肽水平的变化。成年Wistar大鼠静脉注射60 mg/kg剂量的链脲佐菌素,在2-4天内引起胰腺肿胀,胰岛β细胞变性,诱发实验性糖尿病。实验性糖尿病的诱导确实是纯化正常大鼠胰岛细胞用于实验性诱导的糖尿病大鼠睾丸皮下移植的计划的第一步。链脲佐菌素在某些动物中诱导一种类型的糖尿病,其类似于具有非酮症高血糖的糖尿病。为了在体重250-300克(75-90天)的雄性成年大鼠中诱导实验性糖尿病,静脉内注射60 mg/kg的链脲佐菌素。在β细胞变性后三天,在所有动物中诱导糖尿病。将糖尿病动物和正常动物分别饲养在代谢笼中,测量所有动物的体重、摄食量、饮水量、尿量、血糖水平、胰岛素水平和C肽含量,并进行比较。为观察糖尿病大鼠胰岛β细胞的变性,取糖尿病大鼠和正常大鼠胰腺组织,进行染色比较。用链脲佐菌素诱导糖尿病会降低胰岛β细胞中的烟酰胺腺嘌呤二核苷酸(NAD),并导致β细胞中的组织病理学效应,这可能是糖尿病诱导的中间体。本研究采用链脲佐菌素诱发实验性糖尿病。诱导糖尿病后,糖尿病动物的摄食量、饮水量、尿量和血糖均较正常动物增加,但体重、胰岛素和C肽量均较正常动物减少。对糖尿病大鼠和正常大鼠胰腺组织的取样和染色显示,糖尿病大鼠胰岛β细胞已明显变性。在三天内,链脲佐菌素使胰腺肿胀,并最终导致胰岛β细胞变性,诱发实验性糖尿病。与正常大鼠相比,它还改变了糖尿病大鼠的正常代谢。与正常大鼠相比,糖尿病大鼠饮水量、食物量、尿量、血糖增加,而血清胰岛素、C肽和体重下降。
The objective of this study is to induce experimental diabetes mellitus by Streptozotocin in normal adult Wistar rats via comparison of changes in body weight, consumption of food and water, volume of urine and levels of glucose, insulin and C-peptide in serum, between normal and diabetic rats. Intra-venous injection of 60mg/kg dose of Streptozotocin in adult wistar rats, makes pancreas swell and at last causes degeneration in Langerhans islet beta cells and induces experimental diabetes mellitus in the 2-4 days. Induction of experimental diabetes mellitus is indeed the first step in the plan of purification of pancreatic Langerhans islet cells of normal rats for transplanting under the testis subcutaneous of experimentally induced diabetic rats. Streptozotocin induces one type of diabetes which is similar to diabetes mellitus with non-ketosis hyperglycemia in some animal species. For induction of experimental diabetes in male adult rats weighted 250-300 grams (75-90 days), 60mg/kg of Streptozotocin was injected intravenously. Three days after degeneration of beta cells, diabetes was induced in all animals. The diabetic and normal animals were kept in the metabolic cages separately and their body weight, consumption of food and water, urine volume, the levels of serum glucose, insulin and C-peptide quantities in all animals were measured and then these quantities were compared. For a microscopic study of degeneration of Langerhans islet beta cells of diabetic rats, sampling from pancreas tissue of diabetic and normal rats, staining and comparison between them, were done. Induction of diabetes with Streptozotocin decreases Nicotinamide-adenine dinucleotide (NAD) in pancreas islet beta cells and causes histopathological effects in beta cells which probably intermediates induction of diabetes. In this study, we used Streptozotocin for our experiments in induction of experimental diabetes mellitus. After Induction of diabetes, consumption of food and water, volume of urine and glucose increased in the diabetic animals in comparison with normal animals, but the weight of body and the volume of insulin and C-peptide decreased in the diabetic animals. Sampling and staining of pancreas tissue of diabetic and normal rats showed that the Langerhans islet beta cells of diabetic rats have been clearly degenerated. In three days, Streptozotocin makes pancreas swell and at last causes degeneration in Langerhans islet beta cells and induces experimental diabetes. It also changes normal metabolism in diabetic rats in comparison with normal rats. Consumption of water and food, volume of urine, serum glucose increases in diabetic animals in comparison with normal rats but the levels of serum insulin, C-peptide and body weight decreases.