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WNIN/GR-Ob大鼠胰岛对肥胖和胰岛素抵抗的适应性

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats.

作者信息

Singh Himadri, Ganneru Sireesha, Malakapalli Venkata, Chalasani Maniprabha, Nappanveettil Giridharan, Bhonde Ramesh R, Venkatesan Vijayalakshmi

机构信息

a Biochemistry/Stem Cell Research; National Institute of Nutrition; Indian Council of Medical Research ; Hyderabad , India.

出版信息

Islets. 2014;6(5-6):e998099. doi: 10.1080/19382014.2014.998099.

DOI:10.1080/19382014.2014.998099
PMID:25833252
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4398287/
Abstract

WNIN/GR-Ob mutant rat is a novel animal model to study metabolic syndrome (obesity, insulin resistance, hyperinsulinemia, impaired glucose tolerance and cardiovascular diseases). We have investigated the islet characteristics of obese mutants at different age groups (1, 6 and 12 months) to assess the islet changes in response to early and chronic metabolic stress. Our data demonstrates altered islet cell morphology and function (hypertrophy, fibrotic lesions, vacuolation, decreased stimulation index, increased TNFα, ROS and TBARS levels) in mutants as compared to controls. Furthermore, network analysis (gene-gene interaction) studied in pancreas demonstrated increased inflammation as a key factor underlying obesity/metabolic syndrome in mutants. These observations pave way to explore this model to understand islet adaptation in response to metabolic syndrome.

摘要

WNIN/GR-Ob突变大鼠是一种用于研究代谢综合征(肥胖、胰岛素抵抗、高胰岛素血症、糖耐量受损和心血管疾病)的新型动物模型。我们研究了不同年龄组(1、6和12个月)肥胖突变体的胰岛特征,以评估胰岛对早期和慢性代谢应激的变化。我们的数据表明,与对照组相比,突变体的胰岛细胞形态和功能发生了改变(肥大、纤维化病变、空泡化、刺激指数降低、TNFα、ROS和TBARS水平升高)。此外,在胰腺中进行的网络分析(基因-基因相互作用)表明,炎症增加是突变体肥胖/代谢综合征的关键因素。这些观察结果为探索该模型以了解胰岛对代谢综合征的适应性铺平了道路。

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Hyperglycemia induces abnormal gene expression in hematopoietic stem cells and their progeny in diabetic neuropathy.高血糖可诱导糖尿病神经病变中造血干细胞及其后代的异常基因表达。
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Neuron. 2014 Feb 19;81(4):740-54. doi: 10.1016/j.neuron.2014.01.045.
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Leptin gene promoter DNA methylation in WNIN obese mutant rats.瘦素基因启动子 DNA 甲基化在 WNIN 肥胖突变大鼠中的研究。
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