The Effect of Endurance Exercise and Insulin on Akt Phosphorylation in Mices' Hearts and Lungs.

Lee, Hyuek-Jong

Endurance exercise and insulin play key roles in glucose metabolism. Insulin is a stimulator of Akt that is intracellular serine/threonine kinase through activation of the insulin receptor (IR). Akt is known to play a 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 mice's hearts and lungs, C57BL/6J male mice were divided into four groups (C; control group, E; endurance exercise group, I; insulin treatment group, and E+I; endurance exercise and insulin treatment group). Although, Akts in the heart and lung were not phosphorylated in E (17 m/min, 10%), Akt in the 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 increased 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 mice's lungs. This increased IR phosphorylation by endurance exercise may enhance insulin-induced Akt phosphorylation.

EXERCISE; INSULIN; METABOLISM; GLUCOSE; SERINE; APOPTOSIS; PHOSPHORYLATION

International Journal of Applied Sports Sciences, 2004, Vol 16, Issue 1, p55

1598-2939

Academic Journal