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Using high-precision simulation calculations and a semianalytical theory, we finally resolve the controversy over the role of energetic disorder in geminate electron–hole photoseparation in organic solids. We demonstrate that in efficient photovoltaic systems, where the charge-carrier separation probability is high, this probability decreases with increasing disorder, both in the absence and presence of a donor–acceptor heterojunction. This results from energy relaxation of the charged particles in the site energy distribution, which effectively deepens the electron–hole Coulomb well. In inefficient photovoltaic systems, the separation probability also initially decreases but turns into an increasing trend at large disorder. We also demonstrate that in the presence of disorder, the geminate charge-pair separation probability is affected by the mismatch between the electron and hole mobilities, even in homogeneous systems. We show how our theoretical results can be practically applied in an analysis of experimental data in organic photovoltaics.

Type 2 diabetes is characterized by insulin hypersecretion followed by reduced glucose-stimulated insulin secretion (GSIS). Here we show that acute stimulation of pancreatic islets with the insulin secretagogue dextrorphan (DXO) or glibenclamide enhances GSIS, whereas chronic treatment with high concentrations of these drugs reduce GSIS but protect islets from cell death. Bulk RNA sequencing of islets shows increased expression of genes for serine-linked mitochondrial one-carbon metabolism (OCM) after chronic, but not acute, stimulation. In chronically stimulated islets, more glucose is metabolized to serine than to citrate, and the mitochondrial ATP/ADP ratio decreases, whereas the NADPH/NADP+ratio increases. Activating transcription factor-4 (Atf4) is required and sufficient to activate serine-linked mitochondrial OCM genes in islets, with gain- and loss-of-function experiments showing that Atf4 reduces GSIS and is required, but not sufficient, for full DXO-mediated islet protection. In sum, we identify a reversible metabolic pathway that provides islet protection at the expense of secretory function.