ArticleDiabetologia1986
Insulin secretory responses of a clonal cell line of simian virus 40-transformed B cells.
Article in Diabetologia, 1986. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 97 citations in OpenAlex.
- Implanting 1.1B4 human β-cell pseudoislets improves glycaemic control in diabetic severe combined immune deficient mice.World journal of diabetes · 2016Article
- Development and functional characterization of insulin-releasing human pancreatic beta cell lines produced by electrofusion.The Journal of biological chemistry · 2011Article
- Glucose-modulated transgene expression via recombinant adeno-associated virus.Pharmaceutical research · 2002Article
- Isoforms of endoplasmic reticulum Ca(2+)-ATPase are differentially expressed in normal and diabetic islets of Langerhans.The Biochemical journal · 1996Article
- A unique combination of plasma membrane Ca2+-ATPase isoforms is expressed in islets of Langerhans and pancreatic beta-cell lines.The Biochemical journal · 1996Article
- The stimulation of insulin secretion by D-glyceraldehyde correlates with its rate of oxidation in islet cells.The Biochemical journal · 1995Article
- HIT cells secrete β-cell mitogenic factors.Endocrine · 1995Article
- A possible role for glyceraldehyde transport in the stimulation of HIT-T15 insulinoma cells.The Biochemical journal · 1994Article
- Variable regulation by insulin of insulin gene expression in HIT-T15 cells.Diabetologia · 1994Article
- Chronic exposure of HIT cells to high glucose concentrations paradoxically decreases insulin gene transcription and alters binding of insulin gene regulatory protein.The Journal of clinical investigation · 1993Article
- Cyclic adenosine monophosphate prevents the glucocorticoid-mediated inhibition of insulin gene expression in rodent islet cells.The Journal of clinical investigation · 1992Article
- Preservation of insulin mRNA levels and insulin secretion in HIT cells by avoidance of chronic exposure to high glucose concentrations.The Journal of clinical investigation · 1992Article
- Control of insulin gene expression by glucose.The Biochemical journal · 1992Article
- Ca(2+)-activated K+ channels from an insulin-secreting cell line incorporated into planar lipid bilayers.Diabetologia · 1992Article
- Amantadine and sparteine inhibit ATP-regulated K-currents in the insulin-secreting beta-cell line, HIT-T15.British journal of pharmacology · 1991Article
- Characterization of the solubilized glibenclamide receptor in a hamster pancreatic beta-cell line, HIT T15.The Biochemical journal · 1991Article
- Simple empirical assessment of beta-cell function by a constant infusion of glucose test in normal and type 2 (non-insulin-dependent) diabetic subjects.Diabetologia · 1991Article
- Glucose-stimulated insulin release by individual pancreatic beta cells: potentiation by glyburide.Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) · 1991Article
- The beta-cell glibenclamide receptor is an ADP-binding protein.The Biochemical journal · 1990Article
- The role of cytosolic free Ca2+ and protein kinase C in acetylcholine-induced insulin release in the clonal beta-cell line, HIT-T15.The Biochemical journal · 1990Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have evaluated the potential of the clonal insulin-secretory cell line HIT-T15 as a model system for investigating stimulus-secretion coupling in pancreatic B cells. In contrast to other cell lines, HIT cell insulin secretion was consistently stimulated 2- to 3-fold by D-glucose. The maximally effective concentration of glucose was 10 mmol/l; between 2 and 10 mmol/l glucose the increase in insulin release was paralleled by an increased rate of glucose oxidation. The main characteristics of glucose-stimulated insulin release by HIT cells were essentially similar to those of normal islets. Thus, the response was specific for metabolizable sugars (D-mannose and D-glyceraldehyde stimulated insulin release but L-glucose and D-galactose were ineffective); markedly dependent on extracellular Ca2+ concentration; potentiated by forskolin, glucagon, acetylcholine and 12-O-tetradecanoyl phorbol 13-acetate; inhibited by adrenaline or somatostatin; showed a biphasic pattern of release in perifusion experiments, with both phases being potentiated by forskolin. The secretory response of the HIT cells to amino acids was also similar to that of normal islets. Thus, L-leucine and its deamination product 2-ketoisocaproate were effective stimuli, whereas L-isoleucine and L-glutamine were ineffective. Insulin release from HIT cells could also be evoked by the sulphonylureas glibenclamide and tolbutamide and by an increase in concentration of extracellular K+ to 40 mmol/l. The content of cyclic AMP in HIT cells was increased modestly by glucose but not by an increase in extracellular K+. Forskolin elicited a 4-fold increase in cyclic AMP content. We conclude that HIT cells retain the essential features of the insulin secretory response of normal B cells and represent an important tool for further biochemical characterization of the secretory system.
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