Biochemical and biophysical research communications, 2015-08, Vol.464 (1), p.13-19
2015
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- Autor(en) / Beteiligte
- Titel
- Physiological characterization of the human EndoC-βH1 β-cell line
- Ist Teil von
- Biochemical and biophysical research communications, 2015-08, Vol.464 (1), p.13-19
- Ort / Verlag
- United States: Elsevier Inc
- Erscheinungsjahr
- 2015
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- In the new human EndoC-βH1 β-cell line, a detailed analysis of the physiological characteristics was performed. This new human β-cell line expressed all target structures on the gene and protein level, which are crucial for physiological function and insulin secretion induced by glucose and other secretagogues. Glucose influx measurements revealed an excellent uptake capacity of EndoC-βH1 β-cells by the Glut1 and Glut2 glucose transporters. A high expression level of glucokinase enabled efficient glucose phosphorylation, increasing the ATP/ADP ratio along with stimulation of insulin secretion in the physiological glucose concentration range. The EC50 value of glucose for insulin secretion was 10.3 mM. Mannoheptulose, a specific glucokinase inhibitor, blocked glucose-induced insulin secretion (GSIS). The nutrient insulin secretagogues l-leucine and 2-ketoisocaproate also stimulated insulin secretion, with a potentiating effect of l-glutamine. The Kir 6.2 potassium channel blocker glibenclamide and Bay K 8644, an opener of the voltage-sensitive Ca2+ channel significantly potentiated GSIS. Potentiation of GSIS by IBMX and forskolin went along with a strong stimulation of cAMP generation. In conclusion, the new human EndoC-βH1 β-cell line fully mirrors the analogous physiological characteristics of primary mouse, rat and human β-cells. Thus, this new human EndoC-βH1 β-cell line is very well suited for physiological β-cell studies. •The EndoC-βH1 β-cell line is an excellent physiological model of pancreatic human β-cells.•EndoC-βH1 β-cells express all structures required for glucose responsiveness.•EndoC-βH1 β-cells respond to all classical insulin secretory stimuli and inhibitors.•Glucose does not induce IL-1β expression in human EndoC-βH1 β-cells.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0006-291XeISSN: 1090-2104DOI: 10.1016/j.bbrc.2015.05.072Titel-ID: cdi_proquest_miscellaneous_1698030686
- Format
- –
- Schlagworte
- 1-Methyl-3-isobutylxanthine - pharmacology, 3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester - pharmacology, Adenosine Diphosphate - metabolism, Adenosine Triphosphate - biosynthesis, Biological Transport, Calcium Channels - genetics, Calcium Channels - metabolism, Cell Line, Colforsin - pharmacology, Diabetes, Founder Effect, Gene Expression, Glucokinase - antagonists & inhibitors, Glucokinase - genetics, Glucokinase - metabolism, Glucose - metabolism, Glucose responsiveness, Glucose Transporter Type 1 - genetics, Glucose Transporter Type 1 - metabolism, Glucose Transporter Type 2 - genetics, Glucose Transporter Type 2 - metabolism, Glutamine - metabolism, Glutamine - pharmacology, Glyburide - pharmacology, Human EndoC-βH1 β-cells, Humans, Insulin - metabolism, Insulin secretion, Insulin-Secreting Cells - cytology, Insulin-Secreting Cells - physiology, Keto Acids - metabolism, Keto Acids - pharmacology, Leucine - metabolism, Leucine - pharmacology, Mannoheptulose - metabolism, Mannoheptulose - pharmacology, Phosphorylation, Potassium Channels, Inwardly Rectifying - antagonists & inhibitors, Potassium Channels, Inwardly Rectifying - genetics, Potassium Channels, Inwardly Rectifying - metabolism