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. 5.
FIG. 5.

Normal Ca2+ response in FAK-deficient β-cells. A: Intracellular Ca2+ responses, determined by ratiometric Fura-2-AM fluorescence measurements, were similar between RIPcre+fak+/+ and RIPcre+fakfl/fl islets in response to glucose (11 mmol/L) and slightly increased in response to KCl (20 mmol/L). B: There were no differences in baseline or peak Fura-2-AM ratios, fold increase in response to 11 mmol/L glucose, or the time-to-peak response between RIPcre+fak+/+ (□) and RIPcre+fakfl/fl (■) islets; n = 3 mice per genotype. C: Representative traces of voltage-gated Ca2+ currents measured in response to a series of increasing 500-ms depolarizations from −70 mV in single RIPcre+fak+/+ and RIPcre+fakfl/fl β-cells. D: The current-voltage relationship, normalized to cell size, demonstrates a significant increase in Ca2+ current density (○, RIPcre+fak+/+; ●, RIPcre+fakfl/fl), which likely accounts for the increased intracellular Ca2+ response to KCl seen in B; n = 15–17 β-cells from three mice for each genotype. *P < 0.05. Results represent mean ± SE. All mice used in experiments were between 4 and 8 weeks of age. +,+/+, RIPcre+fak+/+; +,−/−, RIPcre fakfl/fl.

This Article

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