体外胰岛素抵抗模型:最新进展。

IF 3.8 Q2 ENDOCRINOLOGY & METABOLISM
Ratih D Yudhani, Yulia Sari, Dwi A A Nugrahaningsih, Eti N Sholikhah, Maftuchah Rochmanti, Abdul K R Purba, Husnul Khotimah, Dian Nugrahenny, Mustofa Mustofa
{"title":"体外胰岛素抵抗模型:最新进展。","authors":"Ratih D Yudhani,&nbsp;Yulia Sari,&nbsp;Dwi A A Nugrahaningsih,&nbsp;Eti N Sholikhah,&nbsp;Maftuchah Rochmanti,&nbsp;Abdul K R Purba,&nbsp;Husnul Khotimah,&nbsp;Dian Nugrahenny,&nbsp;Mustofa Mustofa","doi":"10.1155/2023/1964732","DOIUrl":null,"url":null,"abstract":"<p><p>Insulin resistance, which affects insulin-sensitive tissues, including adipose tissues, skeletal muscle, and the liver, is the central pathophysiological mechanism underlying type 2 diabetes progression. Decreased glucose uptake in insulin-sensitive tissues disrupts insulin signaling pathways, particularly the PI3K/Akt pathway. An <i>in vitro</i> model is appropriate for studying the cellular and molecular mechanisms underlying insulin resistance because it is easy to maintain and the results can be easily reproduced. The application of cell-based models for exploring the pathogenesis of diabetes and insulin resistance as well as for developing drugs for these conditions is well known. However, a comprehensive review of <i>in vitro</i> insulin resistance models is lacking. Therefore, this review was conducted to provide a comprehensive overview and summary of the latest <i>in vitro</i> insulin resistance models, particularly 3T3-L1 (preadipocyte), C2C12 (skeletal muscle), and HepG2 (liver) cell lines induced with palmitic acid, high glucose, or chronic exposure to insulin.</p>","PeriodicalId":16628,"journal":{"name":"Journal of Obesity","volume":null,"pages":null},"PeriodicalIF":3.8000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9876677/pdf/","citationCount":"2","resultStr":"{\"title\":\"<i>In Vitro</i> Insulin Resistance Model: A Recent Update.\",\"authors\":\"Ratih D Yudhani,&nbsp;Yulia Sari,&nbsp;Dwi A A Nugrahaningsih,&nbsp;Eti N Sholikhah,&nbsp;Maftuchah Rochmanti,&nbsp;Abdul K R Purba,&nbsp;Husnul Khotimah,&nbsp;Dian Nugrahenny,&nbsp;Mustofa Mustofa\",\"doi\":\"10.1155/2023/1964732\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Insulin resistance, which affects insulin-sensitive tissues, including adipose tissues, skeletal muscle, and the liver, is the central pathophysiological mechanism underlying type 2 diabetes progression. Decreased glucose uptake in insulin-sensitive tissues disrupts insulin signaling pathways, particularly the PI3K/Akt pathway. An <i>in vitro</i> model is appropriate for studying the cellular and molecular mechanisms underlying insulin resistance because it is easy to maintain and the results can be easily reproduced. The application of cell-based models for exploring the pathogenesis of diabetes and insulin resistance as well as for developing drugs for these conditions is well known. However, a comprehensive review of <i>in vitro</i> insulin resistance models is lacking. Therefore, this review was conducted to provide a comprehensive overview and summary of the latest <i>in vitro</i> insulin resistance models, particularly 3T3-L1 (preadipocyte), C2C12 (skeletal muscle), and HepG2 (liver) cell lines induced with palmitic acid, high glucose, or chronic exposure to insulin.</p>\",\"PeriodicalId\":16628,\"journal\":{\"name\":\"Journal of Obesity\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2023-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9876677/pdf/\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Obesity\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1155/2023/1964732\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Obesity","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1155/2023/1964732","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 2

摘要

胰岛素抵抗影响胰岛素敏感组织,包括脂肪组织、骨骼肌和肝脏,是2型糖尿病进展的主要病理生理机制。胰岛素敏感组织中葡萄糖摄取减少会破坏胰岛素信号通路,特别是PI3K/Akt通路。体外模型是研究胰岛素抵抗的细胞和分子机制的合适方法,因为它易于维持,结果易于复制。应用细胞为基础的模型来探索糖尿病和胰岛素抵抗的发病机制以及开发针对这些疾病的药物是众所周知的。然而,缺乏对体外胰岛素抵抗模型的全面回顾。因此,本综述旨在全面概述和总结最新的体外胰岛素抵抗模型,特别是3T3-L1(前脂肪细胞)、C2C12(骨骼肌)和HepG2(肝)细胞系,这些细胞系由棕榈酸、高糖或慢性胰岛素暴露诱导。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

<i>In Vitro</i> Insulin Resistance Model: A Recent Update.

<i>In Vitro</i> Insulin Resistance Model: A Recent Update.

<i>In Vitro</i> Insulin Resistance Model: A Recent Update.

In Vitro Insulin Resistance Model: A Recent Update.

Insulin resistance, which affects insulin-sensitive tissues, including adipose tissues, skeletal muscle, and the liver, is the central pathophysiological mechanism underlying type 2 diabetes progression. Decreased glucose uptake in insulin-sensitive tissues disrupts insulin signaling pathways, particularly the PI3K/Akt pathway. An in vitro model is appropriate for studying the cellular and molecular mechanisms underlying insulin resistance because it is easy to maintain and the results can be easily reproduced. The application of cell-based models for exploring the pathogenesis of diabetes and insulin resistance as well as for developing drugs for these conditions is well known. However, a comprehensive review of in vitro insulin resistance models is lacking. Therefore, this review was conducted to provide a comprehensive overview and summary of the latest in vitro insulin resistance models, particularly 3T3-L1 (preadipocyte), C2C12 (skeletal muscle), and HepG2 (liver) cell lines induced with palmitic acid, high glucose, or chronic exposure to insulin.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Journal of Obesity
Journal of Obesity ENDOCRINOLOGY & METABOLISM-
CiteScore
7.50
自引率
3.00%
发文量
19
审稿时长
21 weeks
期刊介绍: Journal of Obesity is a peer-reviewed, Open Access journal that provides a multidisciplinary forum for basic and clinical research as well as applied studies in the areas of adipocyte biology & physiology, lipid metabolism, metabolic syndrome, diabetes, paediatric obesity, genetics, behavioural epidemiology, nutrition & eating disorders, exercise & human physiology, weight control and health risks associated with obesity.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信