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. 2019 Aug 5;77(8):1623–1643. doi: 10.1007/s00018-019-03249-4

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© The Author(s) 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Fig. 8 — The mode of action of NPC43 against hyperglycemia and glucose intolerance in diabetes. NPC43 acts as a novel insulin-mimetic small molecule which interacts with extracellular INSRα to selectively activate INSR signaling in both liver and skeletal muscle cells. This leads the inhibition of glucose production and stimulation of glucose uptake. In addition, NPC43 also can cooperate with insulin to further inhibit G6pc expression in hepatocytes and enhance glucose uptake in skeletal muscle cells. More importantly, in insulin-resistant T2D subjects, NPC43 is able to restore INSR function in both liver and skeletal muscle, thereby attenuating hyperglycemia and glucose intolerance