Based on Farah report, insulin can be glycated as monoglycation or diglycation product. Central sites for insulin glycation are B 1-13 and B 22-30 peptide fragment. Since glycation can alter the mobility of insulin molecule, we speculate that slower release of insulin than C-peptides may accordingly occur during insulin secretion by exocytosis of the vesicles. Here we theoretically propose some possibility combinations that insulin secretion can be dependent on many factors: Glycation status of insulin and cargo proteins; ageing process; deficiency of zinc ions; deficiency of calcium ions; the polymeric forms of insulin in vesicles; the ageing related stress with ROS production; the chronic psychological stress; the effect of environmental hormones; and finally the retrograde impairment of insulin release by insulin resistance.
關聯:
International Journal of Molecular Medicine and Advanced Sciences 3(3):108-117
