In Vitro Insulin Resistance Model: A Recent Update

Author:

Yudhani Ratih D.1ORCID,Sari Yulia2ORCID,Nugrahaningsih Dwi A. A.3ORCID,Sholikhah Eti N.3ORCID,Rochmanti Maftuchah4ORCID,Purba Abdul K. R.4ORCID,Khotimah Husnul5ORCID,Nugrahenny Dian5,Mustofa Mustofa3ORCID

Affiliation:

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

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

3. Department of Pharmacology and Therapy, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Jl. Farmako, Sekip Utara, Sleman, Daerah Istimewa Yogyakarta 55281, Indonesia

4. Department of Anatomy, Histology and Pharmacology, Faculty of Medicine, Universitas Airlangga, Jl Mayjen Prof. Dr. Moestopo 47, Surabaya, East Java 60131, Indonesia

5. Department of Pharmacology, Faculty of Medicine, Universitas Brawijaya, Jl. Veteran, Malang, East Java 65145, Indonesia

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 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.

Funder

Indonesian Collaborative Research Grant

Publisher

Hindawi Limited

Subject

Endocrinology, Diabetes and Metabolism

Reference60 articles.

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