4.8 Article

FAK signalling controls insulin sensitivity through regulation of adipocyte survival

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NATURE COMMUNICATIONS
卷 8, 期 -, 页码 -

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NATURE PUBLISHING GROUP
DOI: 10.1038/ncomms14360

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资金

  1. Canadian Institutes of Health Research (CIHR) [MOP-142193, MOP-93707]
  2. Canada Research Chair in Signal Transduction Diabetes Pathogenesis
  3. Eliot Phillipson Clinician Scientist Training Program
  4. Banting and Best Diabetes Centre Postdoctoral Fellowship
  5. Canadian Diabetes Association (CDA)
  6. Canadian Society of Endocrinology and Metabolism Dr Fernand Labrie Fellowship Research Award
  7. Canadian Liver Foundation Graduate Studentship
  8. CDA Doctoral Student Research Award
  9. CIHR-Frederick Banting and Charles Best Canada Graduate Scholarship
  10. Banting and Best Diabetes Centre-Novo Nordisk Studentship

向作者/读者索取更多资源

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 PPAR gamma 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.

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