Cellular stress is a prerequisite for glucose-induced mitochondrial matrix alkalinization in pancreatic β-cells.

摘要: Changes in mitochondrial and cytosolic pH alter the chemical gradient across inner membrane. The proton contributes to ATP synthesis as well uptake release of metabolites ions from organelle. Here ΔpH were studied for first time human pancreatic β-cells. Adenoviruses used rat insulin promoter dependent expression sensor SypHer targeted either matrix or cytosol. resting β-cells is low (pH = 7.50 ± SD 0.17) compared published values other cell types. Consequently, mitochondria small. Glucose stimulation consistently resulted acidification INS-1E insulinoma cells intact islets islet monolayer cultures. We registered with similar kinetics but slightly smaller amplitude cytosol β-cells, thus glucose further reduced ΔpH. Infection high levels adenoviruses caused increase. apoptosis inducer broad-spectrum kinase inhibitor staurosporine had effects on homeostasis. Although alone does not affect pH, increases treated cells. These two cellular stressors normal response