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Mouse Models of Insulin Resistance: What Have We Learned?
Author(s) -
Bunner Anne E,
Barnard Neal D
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1010.7
Subject(s) - insulin resistance , model organism , human insulin , insulin , animal model , organism , type 2 diabetes , insulin receptor , biology , bioinformatics , genetically engineered , diabetes mellitus , relevance (law) , computational biology , medicine , neuroscience , genetics , microbiology and biotechnology , endocrinology , gene , political science , law
Type 2 diabetes (T2D) affects about 26 million adults in the US, and is a leading cause of cardiovascular mortality. Insulin resistance is a core pathology of T2D, and often arises years before diagnosis. In an effort to understand and treat insulin resistance and T2D, basic researchers have used genetically modified mice to identify insulin signaling pathways and attempt to determine the effects of their perturbation. However, despite decades of these inquiries, the pathophysiology of insulin resistance remains controversial, and no pharmacological cure exists. In light of these facts, and the costs of animal research, we reviewed the uses and limitations of genetically engineered mouse models of insulin resistance. We examined the features of several widely employed mouse models and the relevance of results to human patients. These genetically modified mice have important differences from the human patients they model at the molecular, cellular, organ, and whole‐organism level. Much has been learned about signaling pathways in mice, but the mechanistic insights gained are often limited to the species and strain of the experimental animal, rather than generalizable to the human condition. We conclude that the significant barriers to translatability point out the need to transition from mouse models to human‐based studies of T2D.