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胰岛素抵抗模型:最新进展。

Insulin Resistance Model: A Recent Update.

机构信息

Department of Pharmacology, Faculty of Medicine, Universitas Sebelas Maret, Jl. Ir. Sutami No. 36A, Surakarta, Central Java 57126, Indonesia.

Department of Parasitology, Faculty of Medicine, Universitas Sebelas Maret, Jl. Ir. Sutami No. 36A, Surakarta, Central Java 57126, Indonesia.

出版信息

J Obes. 2023 Jan 18;2023:1964732. doi: 10.1155/2023/1964732. eCollection 2023.

Abstract

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 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 insulin resistance models is lacking. Therefore, this review was conducted to provide a comprehensive overview and summary of the latest 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.

摘要

胰岛素抵抗影响包括脂肪组织、骨骼肌和肝脏在内的胰岛素敏感组织,是 2 型糖尿病进展的核心病理生理机制。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。细胞模型是研究胰岛素抵抗的细胞和分子机制的合适模型,因为它易于维持且结果易于重现。细胞模型在探索糖尿病和胰岛素抵抗的发病机制以及开发这些疾病的药物方面的应用是众所周知的。然而,缺乏对胰岛素抵抗模型的全面综述。因此,本综述旨在全面概述和总结最新的胰岛素抵抗模型,特别是用棕榈酸、高葡萄糖或慢性胰岛素暴露诱导的 3T3-L1(前脂肪细胞)、C2C12(骨骼肌)和 HepG2(肝)细胞系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/64a8/9876677/5d4332a3d071/JOBE2023-1964732.001.jpg

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