Mechanisms of Pancreatic β-Cell Death in Type 1 and Type 2 Diabetes

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FIG. 3.
FIG. 3.

High glucose (28 mmol/l) does not induce NF-κB activation and DNA binding in β-cells, as assessed by immunofluorescence using an antibody directed against the p65 NF-κB subunit. FACS-purified rat β-cells were exposed to 10 mmol/l (control, A) or 28 mmol/l glucose (B) for 12–24 h. The data at 12 h are shown here; similar observations were made at 24 h (not shown). As a positive control, cells were exposed to IL-1β (30 units/ml, in medium containing 10 mmol/l glucose [C]) during the last 30 min of culture. NF-κB is located in the cytosol at 10 mmol/l (A) or 28 mmol/l (B) glucose, whereas it translocates to the nucleus after exposure to IL-1β, indicating activation (C). Subcellular NF-κB localization was counted in 200–400 cells using the same experimental conditions as above (D). □, Cytoplasmic NF-κB localization; ▪, nuclear localization. The results are means ± SE of three independent experiments. *P < 0.001 vs. percent nuclear staining in the control by two-sided paired t test (D). Original magnification ×200.

This Article

  1. Diabetes vol. 54 no. suppl 2 S97-S107