Abdullah Sener

TL;DR: It is demonstrated that SGLT2 is expressed in glucagon-secreting alpha cells of the pancreatic islets, and dapagliflozin treatment further promotes glucagon secretion and hepatic gluconeogenesis in healthy mice, thereby limiting the decrease of plasma glucose induced by fasting.

TL;DR: It is proposed that the generation of both NAD(P)H and H+ participates in the coupling of glucose metabolism to distal events in the secretory sequence, especially the ionophoretic process of Ca2+ inward and outward transport, and that changes in these parameters occur in concert with an increased turn-over rate of high-energy phosphate intermediates.

TL;DR: It is proposed that such a coupling between metabolic and cationic events is operative in response to other insulinotropic nutrients and that its time course may be relevant to the phasic aspect of insulin release.

TL;DR: Data is presented consistent with the idea that BCH induces insulin release through the allosteric activation of glutamate dehydrogenase, which is compatible with the fuel hypothesis, which states that the secretory response to nutrient secretagogues depends always on an increase of catabolic fluxes in the islet cells.

TL;DR: The findings suggest that the selective cytotoxicity of alloxan to the pancreatic B cell is attributable to the conjunction of two features: a rapid cellular uptake of the drug and an exquisite sensitivity of the B cell to peroxide.