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. 4.
FIG. 4.

Reduced insulin secretion in FAK-deficient β-cells with normal GLUT2 expression. A: Reduced random insulin level in RIPcre+fakfl/fl (■) compared with RIPcre+fak+/+ littermates (□); n = 6 per genotype. Insulin content (B) and insulin secretion (C) in response to glucose (2.5 or 15 mmol/L), in group of 10 handpicked, similar-sized islets, were equal between RIPcre+fak+/+ (□) and RIPcre+fakfl/fl (■) islets; n = 4 per genotype. D: Reduced insulin secretion in vivo after glucose stimulation in RIPcre+fakfl/fl (▲) compared with RIPcre+fak+/+ littermates (△); n = 5–6 per genotype. E: Normal expression and distribution of GLUT2 on RIPcre+fakfl/fl islets, as assessed by insulin/GLUT2 immunofluorescent costaining (original magnification ×20); n = 3 per genotype. Scale bars, 40 μm. *P < 0.05; **P < 0.01. Results represent mean ± SE. All mice used in experiments were between 4 and 8 weeks of age. +,+/+, RIPcre+fak+/+; +,−/−, RIPcre+fakfl/fl. wks, weeks. (A high-quality digital representation of this figure is available in the online issue.)

This Article

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