FAK signalling controls insulin sensitivity through regulation of adipocyte survival

Cynthia T. Luk, Sally Yu Shi, Erica P. Cai, Tharini Sivasubramaniyam, Mansa Krishnamurthy, Jara J. Brunt, Stephanie A. Schroer, Daniel A. Winer and Minna Woo ()
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Cynthia T. Luk: Toronto General Hospital Research Institute, University Health Network
Sally Yu Shi: Toronto General Hospital Research Institute, University Health Network
Erica P. Cai: Toronto General Hospital Research Institute, University Health Network
Tharini Sivasubramaniyam: Toronto General Hospital Research Institute, University Health Network
Mansa Krishnamurthy: Toronto General Hospital Research Institute, University Health Network
Jara J. Brunt: Toronto General Hospital Research Institute, University Health Network
Stephanie A. Schroer: Toronto General Hospital Research Institute, University Health Network
Daniel A. Winer: Toronto General Hospital Research Institute, University Health Network
Minna Woo: Toronto General Hospital Research Institute, University Health Network

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Focal adhesion kinase (FAK) plays a central role in integrin signalling, which regulates growth and survival of tumours. Here we show that FAK protein levels are increased in adipose tissue of insulin-resistant obese mice and humans. Disruption of adipocyte FAK in mice or in 3T3 L1 cells decreases adipocyte survival. Adipocyte-specific FAK knockout mice display impaired adipose tissue expansion and insulin resistance on prolonged metabolic stress from a high-fat diet or when crossed on an obese db/db or ob/ob genetic background. Treatment of these mice with a PPARγ agonist does not restore adiposity or improve insulin sensitivity. In contrast, inhibition of apoptosis, either genetically or pharmacologically, attenuates adipocyte death, restores normal adiposity and improves insulin sensitivity. Together, these results demonstrate that FAK is required for adipocyte survival and maintenance of insulin sensitivity, particularly in the context of adipose tissue expansion as a result of caloric excess.

Date: 2017
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DOI: 10.1038/ncomms14360

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