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Publication : The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models.

First Author  Joost HG Year  2014
Journal  Mamm Genome Volume  25
Issue  9-10 Pages  401-12
PubMed ID  24752583 Mgi Jnum  J:216848
Mgi Id  MGI:5609763 Doi  10.1007/s00335-014-9514-2
Citation  Joost HG, et al. (2014) The genetic basis of obesity-associated type 2 diabetes (diabesity) in polygenic mouse models. Mamm Genome 25(9-10):401-12
abstractText  Obesity-associated diabetes ("diabesity") in mouse strains is characterized by severe insulin resistance, hyperglycaemia and progressive failure, and loss of beta cells. This condition is observed in inbred obese mouse strains such as the New Zealand Obese (NZO/HlLt and NZO/HlBomDife) or the TALLYHO/JngJ mouse. In lean strains such as C57BLKS/J, BTBR T+tf/J or DBA/2 J carrying diabetes susceptibility genes ("diabetes susceptible" background), it can be induced by introgression of the obesity-causing mutations Lep <ob> (ob) or Lepr <db> (db). Outcross populations of these models have been employed in the genome-wide search for mouse diabetes genes, and have led to positional cloning of the strong candidates Pctp, Tbc1d1, Zfp69, and Ifi202b (NZO-derived obesity) and Sorcs1, Lisch-like, Tomosyn-2, App, Tsc2, and Ube2l6 (obesity caused by the ob or db mutation). Some of these genes have been shown to play a role in the regulation of the human glucose or lipid metabolism. Thus, dissection of the genetic basis of obesity and diabetes in mouse models can identify regulatory mechanisms that are relevant for the human disease.
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