Lena Eliasson

TL;DR: It is shown that overexpression of miR-375 suppressed glucose-induced insulin secretion, and conversely, inhibition of endogenous mi R-375 function enhanced insulin secretion and may constitute a novel pharmacological target for the treatment of diabetes.

TL;DR: Functional analyses demonstrated that identified candidate genes affect pancreatic β- and α-cells as Exoc3l silencing reduced exocytosis and overexpression of Cdkn1a, Pde7b and Sept9 perturbed insulin and glucagon secretion in clonal α- and β-cells, respectively.

TL;DR: The data show that the path from genetic variation (SNP) to gene expression is more complex than hitherto often assumed, and that genetic variation can also influence function of a gene by influencing exon usage or splice isoforms (sQTL), allelic imbalance, RNA editing, and expression of noncoding RNAs.

TL;DR: The evidence that biphasic insulin secretion reflects exocytosis of two functional subsets of secretory granules and the implications for diabetes are reviewed.

TL;DR: Single‐channel recordings confirm that the L‐type Ca2+ channels are clustered in the part of the cell containing the secretory granules, which can be envisaged as being favourable to the B‐cell as it ensures that the Ca2- transient is maximal and restricted to the partof the cell where it is required to rapidly initiate exocytosis.