Endurance exercise and insulin play a key role in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of insulin receptor (IR). Akt is known to play an critical role in promoting cell sur...
Endurance exercise and insulin play a key role in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of insulin receptor (IR). Akt is known to play an critical role in promoting cell survival, inhibiting cell apoptosis, and enhancing glucose uptake and transport. Even though exercise increases glucose transport and glycogen synthesis as insulin does, the relationship of exercise and Akt is not elucidated yet. To determine whether exercise or/and insulin activate Akt in mouse heart and lung, C57BL/6J male mice were divided into four groups (C; control group, E; endurance exercise group, I; insulin treat group, and E+I; endurance exercise and insulin group). Though, Akts in heart and lung were not phosphorylated in E (17 m/min, 10%), Akt in heart and lung was phosphorylated significantly in E+I and I (2.5 unit). Especially, lung Akt phosphorylation in E+I was increased significantly compared with that of I (4.9±0.2 vs 4.0±0.1, p<.05). Furthermore, the lung IR phosphorylation in E+I was increase significantly more than that of I (5.9±0.4 vs 4.5±0.3, p<.05). The increase of lung Akt phosphorylation in E+I was thought to be followed by IR phosphorylation. In conclusion, one hour endurance exercise enhances IR phosphorylation induced by insulin in mouse lung. This increased IR phosphorylation by endurance exercise may enhance insulin-induced Akt phosphorylation.