Altered G<sub>i</sub> signaling in enteroendocrine K cells in vivo causes pronounced changes in glucose homeostasis.

Treatment of STC-1 cells with PKI-14-22 (100 nM), a selective PKA inhibitor, led to a clear trend ( P = 0.104) toward a reduction in glucose-stimulated GIP release ( Fig. 10B ).

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K-GiD mice also showed reduced increases in plasma GIP and insulin levels, although the effect on insulin failed to reach statistical significance (fig.

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