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. 2012 Feb 13;61(3):692–701. doi: 10.2337/db11-1027

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 4. — β₂AR levels, glucose-stimulated insulin secretion, and gene expression profile in silenced INS-1E β-cells. Treatment with a specific β₂AR-shRNA significantly decreased the density (by 73.7% [A]) and mRNA levels (by 59.1% [B]) of β₂AR in INS-1E β-cells. β₂AR-shRNA inhibited the insulin secretory response to 16.7 mmol/L glucose, which was rescued by the overexpression of PPARγ (C). KCl-induced insulin release (C) was not significantly different among the studied groups. β₂AR-shRNA also determined a significant reduction in mRNA level of PDX-1 (D), GLUT2 (E), and PPARγ (F) that was prevented by the overexpression of PPARγ. Bars represent means ± SE from four to five independent experiments in each of which reactions were performed in triplicate (, control, i.e. untreated INS-1E β-cells; , sh-scramble; , sh-scramble+empty vector; , sh-β₂AR; , sh-β₂AR+PPARγ; *P < 0.05 vs. control, Bonferroni post hoc test; basal is glucose 2.8 mmol/L. Equal amount of proteins from three independent experiments was analyzed by Western blotting and quantified by densitometry (G and H ). *P < 0.05 vs. sh-scramble. AU, arbitrary units. (See also Supplementary Figs. 2–4.)

Inline graphic — β₂AR levels, glucose-stimulated insulin secretion, and gene expression profile in silenced INS-1E β-cells. Treatment with a specific β₂AR-shRNA significantly decreased the density (by 73.7% [A]) and mRNA levels (by 59.1% [B]) of β₂AR in INS-1E β-cells. β₂AR-shRNA inhibited the insulin secretory response to 16.7 mmol/L glucose, which was rescued by the overexpression of PPARγ (C). KCl-induced insulin release (C) was not significantly different among the studied groups. β₂AR-shRNA also determined a significant reduction in mRNA level of PDX-1 (D), GLUT2 (E), and PPARγ (F) that was prevented by the overexpression of PPARγ. Bars represent means ± SE from four to five independent experiments in each of which reactions were performed in triplicate (, control, i.e. untreated INS-1E β-cells; , sh-scramble; , sh-scramble+empty vector; , sh-β₂AR; , sh-β₂AR+PPARγ; *P < 0.05 vs. control, Bonferroni post hoc test; basal is glucose 2.8 mmol/L. Equal amount of proteins from three independent experiments was analyzed by Western blotting and quantified by densitometry (G and H ). *P < 0.05 vs. sh-scramble. AU, arbitrary units. (See also Supplementary Figs. 2–4.)