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β-cells

Development of a Scalable Method to Isolate Subsets of Stem Cell-Derived Pancreatic Islet Cells

[Stem Cell Reports] Scientists described the generation of an array of monoclonal antibodies against cell surface markers that selectively label stem cell-derived islet cells.

An HNF1α Truncation Associated with Maturity-Onset Diabetes of the Young Impairs Pancreatic Progenitor Differentiation by Antagonizing HNF1β Function

[Cell Reports] Scientists used maturity-onset diabetes of a young 3 patient and CRISPR/Cas9-engineered human induced pluripotent stem cells (hiPSC) grown as 3D organoids to investigate how HNF1αp291fsinsC affected hiPSC differentiation during pancreatic development.

mPGES-2 Blockade Antagonizes β-Cell Senescence to Ameliorate Diabetes by Acting on NR4A1

[Nature Metabolism] Mechanistically, the protective role of microsomal prostaglandin E synthase-2 (mPGES-2) deletion was induced by antagonizing β-cell senescence via interference of the PGE2–EP3–NR4A1 signaling axis.

Reduced Production of Isoprostanes by Peri-Pancreatic Adipose Tissue from Zucker Fa/Fa Rats as a New Mechanism for β-Cell Compensation in Insulin Resistance and Obesity

[Free Radical Biology and Medicine] Researchers investigated whether peri-pancreatic white adipose tissue produced oxygenated lipids, namely isoprostanes and neuroprostanes and whether they can influence β-cell function in obesity.

Cadmium Exposure Suppresses Insulin Secretion through mtROS-Mediated Mitochondrial Dysfunction and Inflammatory Response in Pancreatic Beta Cells

[Journal of Trace Elements in Medicine and Biology] Scientists used an in vitro MIN6 cell model of environment-relevant cadmium exposure to elucidate the crucial role of mtROS-mediated mitochondrial dysfunction and inflammatory response in suppression of pancreatic β-cell insulin secretion.

Cadmium Exposure Suppresses Insulin Secretion through mtROS-Mediated Mitochondrial Dysfunction and Inflammatory Response in Pancreatic Beta Cells

[Journal of Trace Elements in Medicine and Biology] Scientists used an in vitro MIN6 cell model of environment-relevant cadmium exposure to elucidate the crucial role of mtROS-mediated mitochondrial dysfunction and inflammatory response in suppression of pancreatic β-cell insulin secretion.

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