Abstract
BackgroundTrilobatin, a natural compound, has been found to exhibit anti-diabetic properties in high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic mice. But up to now no research has been reported on the effect of trilobatin on insulin resistance in peripheral tissues. Herein, we determined the effects of trilobatin on insulin resistance in palmitate-treated C2C12 myotubes and ob/ob mice.MethodsMale ob/ob mice (8-10 weeks) and same background C57BL/6 mice were used to evaluate the role of trilobatin on insulin resistance; protein expression and phosphorylation were measured by western blot; glucose uptake was determined a fluorescent test.Results Treatment with trilobatin prevented palmitate-induced insulin resistance by enhancing glucose uptake and the phosphorylation of insulin resistance substrate 1 (IRS1) and protein Kinase B, (PKB/AKT), recovered the translocation of GLUT4 from cytoplasm to membrane, but preincubation with LY294002, an inhibitor of PI3K, blocked the effects of trilobatin on glucose uptake and the distribution of GLUT4 in C2C12 myotubes. Furthermore, administration with trilobatin for 4 weeks significantly improved insulin resistance by decreasing fasting blood glucose and insulin in serum, enhancing the phosphorylation of IRS1 and AKT, and recovering the expression and translocation of GLUT4 in ob/ob mice.ConclusionsIRS-AKT-GLUT4 signaling pathway might be involved in trilobatin ameliorating insulin resistance in skeletal muscle of obese animal models.
Highlights
Trilobatin, a natural compound, has been found to exhibit anti-diabetic properties in high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic mice
Trilobatin prevented the palmitate‐induced decrease of glucose uptake in C2C12 myotubes It has been established that the development of myoblasts is achieved with the expression of some myoblast-specific transcription factors, including myogenic determination protein 1 (MYOD1), myogenic factor 5 (MYF5), myogenin (MYOG) and myogenic factor 6 (MRF6) and some structural and enzymatic musclespecific proteins such as myosin heavy chain 1 (MYH1), the main motor protein in muscle filaments [24]
C2C12 myoblasts were firstly incubated with differentiated media (DMEM supplied with 2% horse serum and 1% P/S) to induce the development of myotubes as described in “Methods”, the results demonstrated that the myoblasts were induced from human fibroblasts, and the myotube-like muti-nuclear structure were developed, which were confirmed by observing the morphology (Additional file 1: Figure S1A), detecting the protein markers MYH1 (Additional file 1: Figure S1B) and MYOD1 (Additional file 1: Figure S1C) of myotubes with western blot assay
Summary
Trilobatin, a natural compound, has been found to exhibit anti-diabetic properties in high-fat diet (HFD) and streptozotocin (STZ) induced type 2 diabetic mice. Up to now no research has been reported on the effect of trilobatin on insulin resistance in peripheral tissues. We determined the effects of trilobatin on insulin resistance in palmitate-treated C2C12 myotubes and ob/ob mice. The role of skeletal muscle in glucose homeostasis has been widely reported in insulin resistance in both cellular and animal disease models [5,6,7]. Trilobatin exhibits anti-hyperglycemic properties by accelerating liver glycogen synthesis, decreasing oxidative stress, increasing the expression of glucokinase, and up-regulating the expression of insulin receptor substrate (IRS) on long-term double high-fat diet and streptozotocin (STZ) induced type 2 diabetic mice [13]. The effect of trilobatin on insulin resistance is still needed to be identified
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