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FAK signalling controls insulin sensitivity through regulation of adipocyte survival

Cynthia T Luk1,2, Sally Yu Shi1,2, Erica P Cai1,2

  • 1Toronto General Hospital Research Institute, University Health Network, MaRS Ctre, TMDT, 101 College Street, 10th Floor, Room 10-363, Toronto, Ontario, Canada M5G 1L7.

Nature Communications
|February 7, 2017
PubMed

Insights

Focal adhesion kinase (FAK) is crucial for fat cell survival and maintaining insulin sensitivity, especially during obesity. Inhibiting apoptosis improves metabolic health in FAK-related conditions.

Area of Science:

  • Cell Biology
  • Metabolic Research
  • Obesity Studies

Background:

  • Focal adhesion kinase (FAK) is integral to integrin signaling, impacting tumor cell growth and survival.
  • Increased FAK protein levels are observed in the adipose tissue of obese individuals with insulin resistance.

Purpose of the Study:

  • To investigate the role of FAK in adipocyte survival and its impact on insulin sensitivity.
  • To determine if targeting FAK or apoptosis pathways can ameliorate insulin resistance in obesity.

Main Methods:

  • Generated adipocyte-specific FAK knockout mice and used 3T3 L1 cells.
  • Administered high-fat diets and utilized obese mouse models (db/db, ob/ob).
  • Tested PPARγ agonist treatment and genetic/pharmacological inhibition of apoptosis.

Main Results:

  • Disruption of adipocyte FAK reduced adipocyte survival and impaired adipose tissue expansion.
  • FAK knockout mice exhibited insulin resistance under metabolic stress.
  • Inhibition of apoptosis, but not PPARγ agonism, restored adiposity and improved insulin sensitivity.

Conclusions:

  • FAK is essential for adipocyte survival and maintaining insulin sensitivity, particularly in obesity-induced adipose tissue expansion.
  • Targeting apoptosis pathways offers a therapeutic strategy for improving insulin sensitivity in conditions of caloric excess.

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