Differentiation-inducing factor-1 (DIF-1) isolated from the cellular slime mold Dictyostelium discoideum has been shown to promote glucose uptake in mouse 3T3-L1 fibroblasts and differentiated 3T3-L1 adipocytes ⁽¹⁾. DIF-1 promotes glucose uptake in the cells, at least in part, via an AMP kinase-dependent pathway (a PI-3 kinase/Akt-independent pathway), which is different from the insulin-induced glucose uptake pathway. In this study, we investigated the actions of DIF-1 in skeletal muscle, the largest glucose-metabolizing tissue, using C2C12 myotube cells.
　During 15 h of incubation, DIF-1 at 1–20 μM promoted glucose consumption (uptake) in a dose-dependent manner in C2C12 myotube cells, while DIF-1 at 10–20 μM was slightly toxic to the cells. DIF-1 (2 μM)-induced glucose consumption was hardly inhibited with wortmannin (0.1 μM), a PI3K inhibitor, but was partially inhibited with compound C (30 μM), an AMP kinase inhibitor. These results suggest that DIF-1 promotes glucose uptake in skeletal muscle cells via the same mechanisms as those in adipocytes and also that DIF-1 may have therapeutic potential in the treatment of obesity and/or diabetes.
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