The recruitment of clathrin to the cup may have a covert purpose to participate in the fission of vesicles from the phagosome during phagosome maturation. The previous study shows that clathrin plays an important role in phagocytosis. In this study, the results indicated that the downregulation of CLTC1 by sequencespecific siRNA resulted in a significant decrease of phagocytic activity in macrophages, showing the involvement of clathrin in phagocytosis. In this context, the miR-1-clathrin interaction revealed in this investigation represented a novel Methylparaben inhibitor mechanism of the regulation of phagocytosis. Incretin based therapy has been clinically applied for the treatment of diabetes. However, the glucose regulating mechanism and potential danger are still less known and under hot discussion. In this study, we used young and aging rodent models to evaluate the potential effect of aging on Glucagon like peptide-1 mimetic exendin-4 therapy. Exendin-4 is a DPPIV resistant GLP-1 receptor agonist. Exendin-4 exerts insulinotropic effects and has multiple glucose regulatory functions through activation of GLP-1 receptor in the mammalian cells. Exendin-4 treatment increases proliferation, neogenesis and survival of beta cells through activation of PKA and AKT with associated gene expression. Treatment with exendin-4 increases Oxprenolol satiety, reduces food intake and slows gastric emptying. In adipocytes, exendin-4 enhances insulin sensitivity and glucose transport by increasing the expression of Insulin Receptor beta, Insulin Receptor Substrate-1 and Glucose Transporter 4. In the murine liver, exendin-4 treatment improves glucose and lipid metabolism, independent of insulin disposal although the exact mechanism remains to be clarified. It was also reported that exendin-4 inhibited hepatocyte and cholangiocyte apoptosis. The risk of diabetes increases with age which is also a risk factor for drug-induced hypoglycemia. Thus, GLP-1 mimetics may be preferred in elderly subjects due to their low risk of hypoglycemia. Despite these theoretical advantages, the effects of aging on incretin therapy have not been well studied. Both beta cell function and proliferation decline with aging and while the GLP-1 mediated acute insulinotropic effect of exendin-4 is maintained in adult and aged rodent, the drug has no effect on beta cell proliferation.