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Inhibition of the glucose transporter SGLT2 with dapagliflozin in pancreatic alpha cells triggers glucagon secretion
TLDR
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. Expand
Involvement of MicroRNAs in the Cytotoxic Effects Exerted by Proinflammatory Cytokines on Pancreatic β-Cells
TLDR
MiR-21, miR-34a, andmiR-146a are identified as novel players in β-cell failure elicited in vitro and in vivo by proinflammatory cytokines, notably during the development of peri-insulitis that precedes overt diabetes in NOD mice. Expand
Alterations in MicroRNA Expression Contribute to Fatty Acid–Induced Pancreatic β-Cell Dysfunction
TLDR
The findings suggest that at least part of the detrimental effects of palmitate on β-cells is caused by alterations in the level of specific miRNAs. Expand
MicroRNAs contribute to compensatory β cell expansion during pregnancy and obesity.
TLDR
Blockade of miR-338-3p in β cells using specific anti-miR molecules mimicked gene expression changes occurring during β cell mass expansion and resulted in increased proliferation and improved survival both in vitro and in vivo. Expand
MicroRNA-9 Controls the Expression of Granuphilin/Slp4 and the Secretory Response of Insulin-producing Cells*
TLDR
Evidence is provided that in insulin-producing cells adequate levels of mir-9 are mandatory for maintaining appropriate Granuphilin levels and optimal secretory capacity, and that silencing of Onecut-2 by RNA interference increases Gran Euphilin expression and mimics the effect of Mir-9 on stimulus-induced exocytosis. Expand
Risk prediction of prevalent diabetes in a Swiss population using a weighted genetic score—the CoLaus Study
TLDR
In this population, a simple weighted 15 SNP-based genetic score provides additional information over clinical predictors of prevalent diabetes, and at this stage, the clinical benefit of this genetic information is limited. Expand
Human high-density lipoprotein particles prevent activation of the JNK pathway induced by human oxidised low-density lipoprotein particles in pancreatic beta cells
TLDR
These data provide strong evidence that oxidised LDL particles exert deleterious effects in the progression of beta cell failure in diabetes and that these effects can be countered by HDL particles. Expand
Functional significance of repressor element 1 silencing transcription factor (REST) target genes in pancreatic beta cells
TLDR
Evidence is provided that the downregulation of these genes is detrimental for the exocytosis of large dense core vesicles, thus contributing to beta cell dysfunction and impaired glucose homeostasis. Expand
Role for inducible cAMP early repressor in promoting pancreatic beta cell dysfunction evoked by oxidative stress in human and rat islets
TLDR
Induction of ICER links oxidative stress to beta cell failure caused by oxidised LDL and can be effectively abrogated by antioxidant treatment, whereas antioxidant treatment with N-acetylcysteine or HDL prevented the rise of ICERN and restored beta cell functions. Expand
Anatomy of a Homeoprotein Revealed by the Analysis of Human MODY3 Mutations*
TLDR
A clear causative relationship between MODY3 mutations and functional defects in HNF1α trans-activation is defined and new light is shed on the structure of a homeoprotein playing a key role in pancreatic β cell function. Expand
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