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. 2013 Apr 16;62(5):1547–1556. doi: 10.2337/db12-1067

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© 2013 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. 1. — G6PC2: a negative regulator of basal GSIS. A: Glucose-6-phosphatase activity was compared in two independent islet preparations isolated from G6pc2 WT and KO mice as described in Research Design and Methods. The results show mean glucose-6-phosphatase activity ± SD. B: A simplified model for GSIS proposing the existence of a glucokinase/G6PC2 futile cycle. The best-characterized pathway for GSIS is shown, although other pathways clearly contribute (40). Overexpression of Gck increases glycolytic flux and results in a leftward shift in the S_0.5 for GSIS (31,32). We hypothesize that G6PC2 is a negative regulator of basal GSIS such that a reduction in G6PC2 expression augments glycolytic flux and causes a leftward shift in the dose-response curve for GSIS. The G6P transporter (G6PT) is a G6P–Pi antiporter (41). ER, endoplasmic reticulum.