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代谢综合征小鼠模型:高脂饮食喂养的 C57BL/6 小鼠的胰岛素抵抗、脂肪肝和非酒精性脂肪性胰腺疾病(NAFPD)。

A Mouse Model of Metabolic Syndrome: Insulin Resistance, Fatty Liver and Non-Alcoholic Fatty Pancreas Disease (NAFPD) in C57BL/6 Mice Fed a High Fat Diet.

机构信息

Laboratory of Morphometry and Cardiovascular Morphology, Biomedical Center, Institute of Biology, State University of Rio de Janeiro, Av 28 de Setembro, 87 (fds) - CEP 20551-030, Rio de Janeiro, Brazil.

出版信息

J Clin Biochem Nutr. 2010 May;46(3):212-23. doi: 10.3164/jcbn.09-83. Epub 2010 Apr 10.

Abstract

Diet-induced obesity in C57BL/6 mice triggers common features of human metabolic syndrome (MetS). The purpose is to assess the suitability of a diet-induced obesity model for investigating non-alcoholic fatty pancreatic disease (NAFPD), fatty liver and insulin resistance. Adult C57BL/6 mice were fed either high-fat chow (HFC, 60% fat) or standard chow (SC, 10% fat) during a 16-week period. We evaluated in both groups: hepatopancreatic injuries, pancreatic islets size, alpha and beta-cell immunodensities, intraperitoneal insulin tolerance test (IPITT) and oral glucose tolerance test (OGTT). The HFC mice displayed greater mass gain (p<0.0001) and total visceral fat pads (p<0.001). OGTT showed impairment of glucose clearance in HFC mice (p<0.0001). IPITT revealed insulin resistance in HFC mice (p<0.0001). The HFC mice showed larger pancreatic islet size and significantly greater alpha and beta-cell immunodensities than SC mice. Pancreas and liver from HFC were heavier and contained higher fat concentration. In conclusion, C57BL/6 mice fed a high-fat diet develop features of NAFPD. Insulin resistance and ectopic accumulation of hepatic fat are well known to occur in MetS. Additionally, the importance of fat accumulation in the pancreas has been recently highlighted. Therefore, this model could help to elucidate target organ alterations associated with metabolic syndrome.

摘要

高脂饮食诱导的 C57BL/6 小鼠肥胖症可引发人类代谢综合征(MetS)的常见特征。本研究旨在评估饮食诱导肥胖模型在研究非酒精性脂肪性胰腺疾病(NAFPD)、脂肪肝和胰岛素抵抗中的适用性。成年 C57BL/6 小鼠在 16 周的时间内分别喂食高脂肪饲料(HFC,60%脂肪)或标准饲料(SC,10%脂肪)。我们在两组中评估了以下指标:肝胰腺损伤、胰腺胰岛大小、α和β细胞免疫密度、腹腔内胰岛素耐量试验(IPITT)和口服葡萄糖耐量试验(OGTT)。HFC 组小鼠表现出更大的体重增加(p<0.0001)和总内脏脂肪垫(p<0.001)。OGTT 显示 HFC 组小鼠葡萄糖清除能力受损(p<0.0001)。IPITT 显示 HFC 组小鼠存在胰岛素抵抗(p<0.0001)。HFC 组小鼠的胰腺胰岛大小明显大于 SC 组小鼠,α和β细胞免疫密度也显著更高。HFC 组的胰腺和肝脏重量更大,脂肪含量更高。总之,高脂饮食喂养的 C57BL/6 小鼠表现出 NAFPD 的特征。胰岛素抵抗和肝脏脂肪异位积累在 MetS 中很常见。此外,最近强调了脂肪在胰腺中的积累的重要性。因此,该模型有助于阐明与代谢综合征相关的靶器官改变。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9774/2872226/b03e787bd70a/jcbn09-83f01.jpg

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