SLC2A4 and diabetes mellitus: In conclusion, our study demonstrates that JTSHF may ameliorate skeletal muscle IR in diabetes mice, and its underlying mechanism may be attributed to stimulate the expression and translocation of GLUT4 by activating the AMPKα/SIRT1/PGC-1α signaling pathway, which not only provides sound scientific evidence for clinical application of the formula, but also offers a new strategy for prevention and treatment of T2DM.