Bcl-2 and Bcl-xL Suppress Glucose Signaling in Pancreatic β-Cells

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FIG. 6.
FIG. 6.

Inducible deletion of Bcl-xL enhances β-cell glucose signaling. A: Quantification of Bcl-xL and Bcl-2 mRNA levels by quantitative PCR (qPCR) (n = 3) and Bcl-xL protein by Western blot (n = 6) in islets from tamoxifen-injected Bcl-xflox/flox:Pdx1-CreER (Bcl-x βKO) mice relative to islets from tamoxifen-injected littermate Bcl-xflox/flox (Bcl-x WT) mice (data are mean ± SEM; *P < 0.05). B: qPCR quantification of Bcl-xL mRNA in hypothalamus from Bcl-xL WT and KO mice (n = 3). C: Percentage of Bcl-x WT and βKO islet cells responding to small-molecule Bcl inhibition (n = 5 mice of each genotype; **P < 0.001 vs. Bcl-x WT). D: Average cytosolic Ca2+ responses of Bcl-x βKO and WT β-cells stimulated with increasing glucose concentrations (Conc.). Shaded hanging bars represent SEM. E: Incremental area under the curve of Ca2+ responses. F: Integrated Ca2+ responses of Bcl-x KO and Bcl-x WT β-cells depolarized with 30 mmol/L KCl (n = 66 Bcl-x WT cells; n = 73 Bcl-x KO cells; three mice per genotype; **P < 0.001). G: Integrated NAD(P)H increases of intact islets following glucose stimulation (n = 11 islets, two mice of each genotype; *P < 0.05). H: Glucose oxidation rates in cultures of dispersed Bcl-xL WT and KO islet cells (n = 4). I: Insulin secretion from perifused Bcl-x WT and KO islets (n = 5). a.u., arbitrary units. (A high-quality color representation of this figure is available in the online issue.)

This Article

  1. Diabetes vol. 62 no. 1 170-182