Fig. 7From: Wnt3a upregulates brain-derived insulin by increasing NeuroD1 via Wnt/β-catenin signaling in the hypothalamusThe proposed regulatory mechanism of insulin expression by the Wnt/β-catenin/NeuroD1 pathway in the hypothalamus. Wnt3a might bind to LRP and Frizzed receptor to activate the canonical Wnt pathway. GSK3 phosphorylates β-catenin and induces its degradation; Wnt3a inhibits GSK3, leading to β-catenin accumulation. Accumulated β-catenin translocates into the nucleus and enhances the expression of NeuroD1 with TCF. Up-regulated NeuroD1 also translocates into the nucleus, where it induces the production of insulinBack to article page