The pores in the cytoplasmic membrane might be indicative of the exocytosis process through which the hormone is released into the extracellular space. Simultaneously, we used AFM to compare the cell membrane particle size and Ra of the membrane surface PF2341066 before or after glucose VRT752271 in vitro stimulation of IPCs and beta cells. Our results revealed that both membrane particle size and Ra of beta cells were larger than those of IPCs. When both two groups of endocrine cells were stimulated by glucose, the membrane particle size and Ra were higher than those not stimulated, except for IPCs that were stimulated for 30 min with low glucose concentration. The magnitude of cellular

Ra, as well as the types, structure, and quantity of membrane protein molecules, directly influenced the inclines and declines of the membrane surface [23]. We speculated that the reason for the lower membrane particle size and Ra in IPCs might be due to their lower membrane protein content. The cell membrane accomplishes its biological

function through membrane liquidity, and exocytosis is one of the functions that depend on membrane liquidity [24, 25]. IPCs and beta cells secreted insulin through exocytosis. selleck chemical In the meantime, their plasma membranes were replenished via membrane liquidity. We inferred that the change in membrane liquidity might cause the increase in cell membrane particle size and Ra after glucose stimulation. Beta cells secrete insulin through exocytosis. In beta cells, actin filaments form a dense network under plasma membrane. This actin network acts as

a barricade, preventing passive diffusion of insulin follicles to the plasma membrane. Thus, the actin network ultimately lessens insulin secretion via reduction of exocytosis [26]. On the contrary, F-actin depolymerization can increase exocytosis, which increases insulin secretion. We proposed that the pores we observed that were located in the cytoplasmic membrane were one of the characteristics of insulin exocytosis, and increased evidence of porous structures may be related to the enhancement of insulin exocytosis. To prove that exocytosis had been enhanced after glucose stimulation of IPCs and beta cells, we demonstrated that without glucose stimulation, the actin network underneath the plasma Ribonucleotide reductase membrane was continuous and dense. After glucose stimulation, the actin network depolymerized and became discontinuous. After F-actin depolymerization, inhibition of exocytosis was relieved and insulin secretion increased. Interestingly, in the IPCs group, the cortical actin network did not depolymerize in low glucose concentrations after 30 min of stimulation. The actin network became discontinuous and depolymerized only after low-glucose stimulation for 1 h. Conclusions In conclusion, our data proved that only normal human pancreatic beta cells could release insulin after low- and high-glucose stimulation for 30 min and 1 h.