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改良高蔗糖饮食诱导的腹部肥胖和正常体重大鼠表现出高血浆游离脂肪酸和胰岛素抵抗。

Modified high-sucrose diet-induced abdominally obese and normal-weight rats developed high plasma free fatty acid and insulin resistance.

机构信息

Division of Geriatrics, West China Hospital of Sichuan University, Chengdu 610041, China.

出版信息

Oxid Med Cell Longev. 2012;2012:374346. doi: 10.1155/2012/374346. Epub 2012 Dec 25.

DOI:10.1155/2012/374346
PMID:23320128
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3540965/
Abstract

INTRODUCTION

Metabolically obese but normal-weight (MONW) individuals have metabolic features of overt obesity, and abdominal adiposity is common in them. Animal models of MONW individuals are lacking. We aimed to develop an abdominally obese and normal-weight (AONW) rat model.

METHODS AND RESULTS

Young male Sprague-Dawley rats were fed chow or a modified high-sucrose (HS) diet for 20 weeks. The HS diet induced increased visceral adipose tissue without increased body weight, reduced glucose disposal rates, and increased hepatic glucose output during the hyperinsulinemic-euglycemic clamp, increased plasma glucose during the intraperitoneal glucose tolerance test, and increased plasma free fatty acids. Hepatic lipidosis and hepatocyte mitochondria swelling were found in HS rats through light microscopy and transmission electron microscopy; similar impairments were not observed in muscle. RT-PCR showed that mRNA expression of uncoupling protein 3 and peroxisome proliferator-activated receptor-gamma coactivator 1α increased in muscle of HS rats, while expression of mitochondrial transcription factor A, glucose transporter type 4, and insulin receptor substrate-1 did not change significantly.

CONCLUSION

AONW rats developed metabolic disorders seen in MONW individuals. Steatosis, mitochondrial morphologic changes, and insulin resistance were more serious in liver than in muscle. Genes involved in fatty acid metabolism and mitochondrial function changed in less impaired muscle.

摘要

简介

代谢肥胖但体重正常(MONW)个体具有明显肥胖的代谢特征,并且腹部肥胖在他们中很常见。MONW 个体的动物模型缺乏。我们旨在开发一种腹部肥胖和体重正常(AONW)大鼠模型。

方法和结果

年轻雄性 Sprague-Dawley 大鼠喂食标准饲料或改良高蔗糖(HS)饮食 20 周。HS 饮食诱导内脏脂肪组织增加而体重增加,葡萄糖处置率降低,在高胰岛素-正常血糖钳夹期间肝葡萄糖输出增加,腹腔内葡萄糖耐量试验期间血浆葡萄糖增加,游离脂肪酸增加。通过光镜和透射电镜观察到 HS 大鼠存在肝脂肪变性和肝细胞线粒体肿胀;在肌肉中未观察到类似的损伤。RT-PCR 显示 HS 大鼠肌肉中解偶联蛋白 3 和过氧化物酶体增殖物激活受体-γ共激活因子 1α 的 mRNA 表达增加,而线粒体转录因子 A、葡萄糖转运蛋白 4 和胰岛素受体底物-1 的表达没有明显变化。

结论

AONW 大鼠出现了 MONW 个体中出现的代谢紊乱。肝内脂肪变性、线粒体形态变化和胰岛素抵抗比肌肉更严重。在受损较轻的肌肉中,参与脂肪酸代谢和线粒体功能的基因发生了变化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/ae53aa48e282/OXIMED2012-374346.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/810e59af4533/OXIMED2012-374346.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/ae53aa48e282/OXIMED2012-374346.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/810e59af4533/OXIMED2012-374346.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/adbc2e1bec58/OXIMED2012-374346.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/0a943606fd72/OXIMED2012-374346.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/b79127a66650/OXIMED2012-374346.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/3734488fa779/OXIMED2012-374346.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/6d14f48aa2af/OXIMED2012-374346.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d8a8/3540965/ae53aa48e282/OXIMED2012-374346.008.jpg

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