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

Lipotoxic, glucotoxic, and glucolipotoxic conditions applied to human islets induced specific expression changes in solute mitochondrial carriers and associated genes, TOM/TIM

To investigate the role of Ca2+ in mitochondrial function, insulin secretion from INS-1 cells stably expressing the Ca2+-sensitive photoprotein aequorin in the appropriate

In intact INS-1 cells stimulated with methyl succinate, the blunted in- sulin secretion correlated with an inhibited increase in [Ca 21 ] m upon a second exposure.. In contrast,

1531. glucose can still cause insulin secretion in the presence of diazoxide, provided that [Ca29~ is raised to a permissive level by membrane depolarization with KCI, thereby

Our results show that the defec- tive glucose-induced insulin secretion observed after H 2 O 2 treatment correlates with altered mitochondrial activation seen as a loss of

Irrespective of the glutamate levels measured in glucose- stimulated cells, the principal observation is that glutamate directly stimulates insulin exocytosis in permeabilised cells

F IG. Induction of WT-HNF1␣ and DN-HNF1␣ regulates the HNF1␣ mRNA expression and HNF1␣ promoter luciferase activity through altered HNF4 ␣ binding. A, for EMSA, the

Cells overexpressing GAD follow- ing AdCA-GAD65 infection and stimulation with high glucose could therefore theoretically release significant amounts of GABA with a possible