Piper methysticum (PM) 在台灣、中國和日本等地為廣泛應用於傳統藥物及保健食品之用途，且具有抗氧化，抗發炎，抗癌等功效。本研究目的為： (i) 探討自PM中獲得的生物活性成分–Flavokawain A (FKA) 在經由棕櫚酸 (PA) 誘導C2C12小鼠骨骼肌細胞後的抗糖尿病及抗發炎效能，與 (ii) 在PA誘導下，FKA對胰島素訊息、Akt/PI3K、MAPKs及GLUT4分子機制之影響。研究結果顯示，10至30 μM FKA能顯著升調節葡萄糖的吸收並增加細胞生長。由PA誘導後加入30 μM FKA除了能顯著升調節葡萄糖吸收外，可降低ROS生成，並降調節NFκB的表現量。在PA誘導後對細胞產生影響，並會使細胞存活率降至81.80%，而在FKA作用下可使細胞存活率達100%，達到保護細胞之效果。經由PA誘導後加入30 μM FKA可以顯著升調節GLUT-4表現，並降調節活化JNK、p38與ERK蛋白質之表現及抑制ROS生成與降低NFκB之表現量。 Piper methysticum (PM) in Taiwan, China and Japan, etc. PM is popularly used as traditional medicines and health foods for antioxidant, anti-inflammatory and anti-cancer effects. In this study, our aims were (i) to examine the anti-diabetic and anti-inflammatory effects of a PM bioactive compound, flavokawain A (FKA) in palmitate (PA)-induced murine C2C12 skeletal muscle cells, and (ii) examine the effect of FKA on insulin, Akt/PI3K, MAPKs and GLUT-4 molecular mechanism (s) in PA-induced cells. As 10 to 30 μM FKA significantly up-regulated the glucose absorption and increased the cell growth. 30 μM FKA significantly up-regulated the glucose up-take, down-regulated ROS formation, as well as decreased the expression of NFκB in PA-induced cells. Results showed that only PA-treated cells, cell viability reduced to 81.80%, but FKA protected the cells to 100%. Co-treatment of cells with PA plus 30 μM FKA significantly up-regulated GLUT-4, down-regulated the activation of JNK, p38 and ERK proteins as well as inhibited the formation of ROS and decreased the levels of NFκB.