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β-cells

ATP Is an Essential Autocrine Factor for Pancreatic β-Cell Signaling and Insulin Secretion

[Physiological Reports] Scientists monitored changes of the intracellular Ca2+ concentration as an immediate read-out for insulin secretion in live cell experiments.

LDB1-Mediated Transcriptional Complexes Are Sensitive to Islet Stress

[Islets] The authors hypothesized that LDB1 and/or ISL1 levels, like other transcriptional regulators, are sensitive to β-cell nutrient and cytokine stresses, likely contributing to β-cell (dys)function under various stimuli.

Clenbuterol Exerts Antidiabetic Activity through Metabolic Reprogramming of Skeletal Muscle Cells

[Nature Communications] To elucidate the underlying cellular and molecular mechanisms, researchers chronically treated wild-type mice and several newly developed mutant mouse strains with clenbuterol, a selective β2-adrenergic receptor agonist.

Exposure to Perfluorooctane Sulfonate Reduced Cell Viability and Insulin Release Capacity of β Cells

[Journal of Environmental Sciences] In a cell-based in vitro bioassay, scientists used mouse β-TC-6 cancer cells and found 48-hour exposure to perfluorooctane sulfonate (PFOS) decreased the cell viability at 50 μmol/L. By measuring insulin content in supernatant, 48-hour pretreatment of PFOS (100 μmol/L) decreased the insulin release capacity of β-TC-6 cells after glucose stimulation.

Cyanidin-3-Rutinoside Stimulated Insulin Secretion through Activation of L-type Voltage-Dependent Ca2+ Channels and the PLC-IP3 Pathway in Pancreatic β-Cells

[Biomedicine & Pharmacotherapy] Scientists identified cyanidin-3-rutinoside's (C3R) mechanisms of action in pancreatic β-cells. Rat INS-1 cells were used to elucidate the effects of C3R on insulin secretion, intracellular Ca2+ signaling, and gene expression.

Intra-Islet Glucagon Confers β-Cell Glucose Competence for First-Phase Insulin Secretion and Favors GLP-1R Stimulation by Exogenous Glucagon

[Journal of Biological Chemistry] Researchers reported that intra-islet glucagon secreted from α-cells signals through β-cell glucagon and GLP-1 receptors, thereby conferring to rat islets their competence to exhibit first phase glucose-stimulated insulin secretion.

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