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. 2018 Dec 21;8(1):6. doi: 10.3390/cells8010006

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Proposed scheme for the glucose uptake-promoting effect of DIFs. Stimulation with a DIF induces glucose transporter 1 (GLUT1) translocation from intracellular vesicles to the plasma membrane (PM) via a PI3K–Akt-independent pathway, resulting in the promotion of glucose uptake by confluent mammalian cells [84]; the DIFs activate PI3K and Akt but this is not related to the DIF glucose uptake-promoting activity [84]. The DIFs also function as mitochondrial uncouplers, promoting oxygen consumption [77] and glucose metabolism (glycolysis and subsequent degradation in the tricarboxylic acid (TCA) cycle) [85] by mitochondria; this further increases GLUT1 translocation and promotes glucose uptake into the cells. Chemical structure-activity relationship analysis revealed that DIF-1 and DIF-1_(3M) are promising lead compounds for the development of anti-diabetes and anti-obesity drugs [71,84,85].