Changes In [Ca～(2+)]i Induced By Insulin In C2C12 Myotubes

Skeletal muscle is the most important tissue that uptakes glucose, whose normal glycometabolism stabilizes the internal environment invivo. Great attentions have been paid on the signal transduction pathwaysof glucose transport. It is said that the glucose transport mechanismsinduced by insulin and contraction are absolutely different, the glucoseuptake stimulated by insulin is dependent on the activation of PI3K, whilethe other is controlled by Ca²⁺ and AMPK. However, recently it has beenfound that Ca²⁺ at a certain concentration attends the glucose transportstimulated by insulin. As is follows: 1. Nifedipine, the blocker of L-typecalcium channels, reduces the glucose uptake induced by insulin inskeletal muscle. 2. Insulin can stimulate the open of L-type calciumchannels and increase the concentration of Ca²⁺ in the cytoplasm. 3. Acertain concentration of calcium plays a role in insulin-stimulatedGLUT4 translocation and exocytosis.In the present study, we build a differentiation model of C2C12myoblasts and then study if Ca²⁺ functions in the signal transductionpathways of glucose transport induced by insulin in skeletal muscles andwhen it functions, we should know what its resources are. Now the studyis divided into two parts: 1. With the method of serum starvation, we successfully differentiateC2C12 myoblasts into mature skeletal muscle cells and then verify themfrom morphological and structural studies.2. Based on the mature skeletal muscle cells, we studied the functionsof Ca²⁺ in insulin transduction pathways. With the application of blockerswe know that insulin stimulates the increases of Ca²⁺ through L-typecalcium channels in the plasma membrane and this process has fewrelationships with the sarcoplasmic reticulum.The present study focuses on the role of Ca²⁺ induced by insulin inskeletal muscle cells to further explain the insulin transduction pathways.