Field-induced water electrolysis switches an oxide semiconductor from an insulator to a metal

Here we demonstrate that water-infiltrated nanoporous glass electrically switches an oxide semiconductor from an insulator to metal. We fabricated the field effect transistor structure on an oxide semiconductor, SrTiO3, using 100%-water-infiltrated nanoporous glass - amorphous 12CaO*7Al2O3 - as the gate insulator. For positive gate voltage, electron accumulation, water electrolysis and electrochemical reduction occur successively on the SrTiO3 surface at room temperature, leading to the formation of a thin (~3 nm) metal layer with an extremely high electron concentration of 10^15-10^16 cm^-2, which exhibits exotic thermoelectric behaviour.Comment: 21 pages, 12 figure

Mitochondrial glutamate acts as a messenger in glucose-induced insulin exocytosis

The hormone insulin is stored in secretory granules and released from the pancreatic beta-cells by exocytosis. In the consensus model of glucose-stimulated insulin secretion, ATP is generated by mitochondrial metabolism, promoting closure of ATP-sensitive potassium (KATP) channels, which depolarizes the plasma membrane. Subsequently, opening of voltage-sensitive Ca2+ channels increases the cytosolic Ca2+ concentration ([Ca2+]c) which constitutes the main trigger initiating insulin exocytosis. Nevertheless, the Ca2+ signal alone is not sufficient for sustained secretion. Furthermore, glucose elicits a secretory response under conditions of clamped, elevated [Ca2+]c. A mitochondrial messenger must therefore exist which is distinct from ATP. We have now identified this as glutamate. We show that glucose generates glutamate from beta-cell mitochondria. A membrane-permeant glutamate analogue sensitizes the glucose-evoked secretory response, acting downstream of mitochondrial metabolism. In permeabilized cells, under conditions of fixed [Ca2+]c, added glutamate directly stimulates insulin exocytosis, independently of mitochondrial function. Glutamate uptake by the secretory granules is likely to be involved, as inhibitors of vesicular glutamate transport suppress the glutamate-evoked exocytosis. These results demonstrate that glutamate acts as an intracellular messenger that couples glucose metabolism to insulin secretion