Fig. 9

Summary of insulin action on NKCC and CFTR participating in epithelial Cl⁻ secretion in epithelial A6 cells. (1) Insulin activates PI3K, resulting in stimulation of NKCC mRNA expression. (2) Insulin inactivates ERK, which suppresses CFTR mRNA expression. Insulin-induced inactivation of ERK releases suppression of CFTR mRNA expression, leading to elevation of CFTR mRNA expression. Both elevation of mRNA expression of NKCC and CFTR induced by insulin stimulates expression of NKCC and CFTR proteins, which stay in cytosolic store sites. cAMP stimulates translocation of insulin-induced NKCC and CFTR proteins staying in cytosolic store sites, leading to much larger epithelial Cl⁻ secretion associated with much larger elevation of CFTR activity than that under the insulin-untreated condition