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低碳水化合物生酮饮食可预防用链脲佐菌素诱导大鼠患糖尿病。

Low carbohydrate ketogenic diet prevents the induction of diabetes using streptozotocin in rats.

作者信息

Al-Khalifa A, Mathew T C, Al-Zaid N S, Mathew E, Dashti H

机构信息

Department of Anatomy, Faculty of Medicine, Health Sciences Center, Kuwait University, Kuwait.

出版信息

Exp Toxicol Pathol. 2011 Nov;63(7-8):663-9. doi: 10.1016/j.etp.2010.05.008. Epub 2010 Jun 18.

Abstract

Diabetes continues to be an overwhelmingly prevalent endocrine disorder that leads to several micro- and macrocomplications. It has been widely accepted that changes in dietary habits could induce or prevent the onset of diabetes. It is shown that low carbohydrate ketogenic diet (LCKD) is effective in the amelioration of many of the deleterious consequences of diabetes. However, its role in preventing the onset of diabetes is not understood. Therefore, this study is focused on the effect of LCKD in preventing the induction of diabetes using streptozotocin (STZ) in rats by biochemical and histological methods. Forty-two Wistar rats weighing 150-250 g were used in this study. The animals were divided into three groups: normal diet (ND), low carbohydrate ketogenic diet (LCKD), and high carbohydrate diet (HCD). Specific diets ad libitum were given to each group of animals for a period of 8 weeks. Each group was further subdivided into normal control, sham control and diabetic groups. Animals in the diabetic group were given a single intraperitoneal injection of STZ (55 mg/kg). All the animals were sacrificed 4 weeks after the injection of STZ. Daily measurements of food and water intake as well as weekly measurement of body weight were taken during the whole 12 weeks of the experiment. After injecting with STZ, the blood glucose level of all the groups increased significantly except for the group fed on LCKD (p value<0.01). Also, food intake, water intake and urine output were significantly increased in all groups except for the LCKD group (p value<0.01). There was also a significant decrease in the weight gain of the animals that were fed on a LCKD as compared to other groups (p value<0.05). Although, substantial decrease in the number of β cells was noticed in diabetic rats, there were no change in the number of β cells in the LCKD treated diabetic animals as compared to LCKD control group. The results presented in this study, therefore, suggests that LCKD prevents the development of diabetes using streptozotocin in rats.

摘要

糖尿病仍然是一种极为普遍的内分泌疾病,会引发多种微血管和大血管并发症。人们普遍认为饮食习惯的改变可能诱发或预防糖尿病的发生。研究表明,低碳水化合物生酮饮食(LCKD)对改善糖尿病的许多有害后果有效。然而,其在预防糖尿病发病方面的作用尚不清楚。因此,本研究通过生化和组织学方法,聚焦于LCKD对使用链脲佐菌素(STZ)诱导大鼠患糖尿病的预防作用。本研究使用了42只体重在150 - 250克的Wistar大鼠。动物被分为三组:正常饮食(ND)组、低碳水化合物生酮饮食(LCKD)组和高碳水化合物饮食(HCD)组。每组动物自由摄取特定饮食,持续8周。每组再进一步细分为正常对照组、假手术对照组和糖尿病组。糖尿病组动物接受单次腹腔注射STZ(55毫克/千克)。注射STZ 4周后处死所有动物。在整个12周的实验过程中,每日测量食物和水的摄入量,每周测量体重。注射STZ后,除LCKD喂养组外,所有组的血糖水平均显著升高(p值<0.01)。此外,除LCKD组外,所有组的食物摄入量、水摄入量和尿量均显著增加(p值<0.01)。与其他组相比,LCKD喂养的动物体重增加也显著减少(p值<0.05)。虽然在糖尿病大鼠中观察到β细胞数量大幅减少,但与LCKD对照组相比,LCKD治疗的糖尿病动物的β细胞数量没有变化。因此,本研究结果表明,LCKD可预防链脲佐菌素诱导的大鼠糖尿病的发生。

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