In Vivo Role of Focal Adhesion Kinase in Regulating Pancreatic β-Cell Mass and Function Through Insulin Signaling, Actin Dynamics, and Granule Trafficking

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FIG. 1.
FIG. 1.

Specific deletion of FAK in the pancreatic β-cells causes glucose intolerance without changes in insulin sensitivity. A: FAK expression in protein lysates of isolated islets of RIPcre+fakfl/fl mice. The expression was not affected in liver, muscle, and hypothalamus between RIPcre+fakfl/fl (■) and RIPcre+fak+/+ mice (□), as shown by Western blot; n = 3 per genotype. GAPDH, glyceraldehyde-3-phosphate dehydrogenase. B: Similar body weight between RIPcre+fak+/+ (□) and RIPcre+fakfl/fl mice (■); n >10 per genotype. C: Increased random blood glucose levels in RIPcre+fakfl/fl mice (■) compared with RIPcre+fak+/+ (□); n = 5 per genotype. D: RIPcre+fakfl/fl mice display glucose intolerance compared with RIPcre+fak+/+ littermates in both age-groups, as assessed by GTT; n = 7–10 per genotype. E: Similar peripheral insulin sensitivity as assessed by insulin tolerance test between RIPcre+fak+/+ and RIPcre+fakfl/fl mice; n = 10 per genotype. △, 4–8-week-old RIPcre+fak+/+; ▲, 4–8-week-old RIPcre+fakfl/fl; □, 12–18-week-old RIPcre+fak+/+; ■, 12–18-week-old RIPcre+fakfl/fl. *Comparison between 4–8-week-old RIPcre+fak+/+ and RIPcre+fakfl/fl islets. #Comparison between 12–18-week-old RIPcre+fak+/+ and RIPcre+fakfl/fl islets. *,#P < 0.05; **P < 0.01; ***P < 0.001. Results represent mean ± SE. +,+/+RIPcre+ fak+/+; +,−/−RIPcre+ fakfl/fl.

This Article

  1. Diabetes vol. 61 no. 7 1708-1718