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. 2013 Feb 14;62(3):789–800. doi: 10.2337/db12-0365

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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. 7. — A diagram shows the existence of positive feedback between the Wnt and GLP-1/cAMP signaling pathways in the brainstem and hypothalamus. In the brainstem, β-cat/TCF7L2 positively regulates gcg expression and the production of GLP-1, which inhibits food intake at least partially by attenuating hypothalamic AMPK activity (26). GLP-1 also stimulates brain Wnt activity via increasing β-cat Ser675 phosphorylation and, possibly, TCF7L2 production. In the brainstem, this leads to increased gcg expression (positive feedback), whereas in hypothalamic neurons this is among the anorectic effects of GLP-1. How the hypothalamic Wnt activation modulates peripheral glucose homeostasis and insulin signaling is currently unknown. (A high-quality color representation of this figure is available in the online issue.)