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Pancreatic beta cell line MIN6 exhibits characteristics of glucose metabolism and glucose-stimulated insulin secretion similar to those of normal islets.

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TLDR
Glucose-stimulated insulin secretion, glucose transport, glucose phosphorylation and glucose utilization have been characterized in the insulinoma cell line MIN6, indicating that this cell line is an appropriate model for studying the mechanism of glucose- stimulated insulin secretion in pancreatic beta cells.
Abstract
Glucose-stimulated insulin secretion, glucose transport, glucose phosphorylation and glucose utilization have been characterized in the insulinoma cell line MIN6, which is derived from a transgenic mouse expressing the large T-antigen of SV40 in pancreatic beta cells. Glucose-stimulated insulin secretion occurred progressively from 5 mmol/l glucose, reached the maximal level approximately seven-fold above the basal level at 25 mmol/l, and remained at this level up to 50 mmol/l. Glucose transport was very rapid with the half-maximal uptake of 3-O-methyl-d-glucose being reached within 15 s at 22 °C. Glucose phosphorylating activity in the cell homogenate was due mainly to glucokinase; the Vmax value of glucokinase activity was estimated to be 255±37 nmol·h−1·mg protein−1, constituting approximately 80% of total phosphorylating activity, whereas hexokinase activity constituted less than 20%. MIN6 cells exhibited mainly the high Km component of glucose utilization with a Vmax of 289±18 nmol·h−1·mg protein−1. Thus, glucose utilization quantitatively and qualitatively reflected glucose phosphorylation in MIN6 cells. In contrast, MIN7 cells, which exhibited only a small increase in insulin secretion in response to glucose, had 4.7-fold greater hexokinase activity than MIN6 cells with a comparable activity of glucokinase. These characteristics in MIN6 cells are very similar to those of isolated islets, indicating that this cell line is an appropriate model for studying the mechanism of glucose-stimulated insulin secretion in pancreatic beta cells.

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Glucose sensitivity and metabolism-secretion coupling studied during two-year continuous culture in INS-1E insulinoma cells

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A Novel Glucose-Sensing Mechanism Contributing to Glucagon-Like Peptide-1 Secretion From the GLUTag Cell Line

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References
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Journal ArticleDOI

Establishment of a pancreatic beta cell line that retains glucose-inducible insulin secretion: special reference to expression of glucose transporter isoforms

TL;DR: The MIN6 cell line will be especially useful to analyze the molecular mechanisms by which beta cells regulate insulin secretion in response to extracellular glucose concentrations, and a possible role of GT isoforms in glucose sensing by beta cells is discussed.
Journal ArticleDOI

Establishment of 2-mercaptoethanol-dependent differentiated insulin-secreting cell lines.

TL;DR: New insulin-secreting cell lines established from cells isolated from an x-ray-induced rat transplantable insulinoma indicate that INS-1 cells have remained stable and retain a high degree of differentiation which should make them a suitable model for studying various aspects of beta-cell function.
Journal ArticleDOI

Cloning and functional expression in bacteria of a novel glucose transporter present in liver, intestine, kidney, and β-pancreatic islet cells

TL;DR: Insulinoma cells express, inappropriately, the erythrocyte glucose transporter, and it is suggested that this may be related to their inability to secrete insulin in response to elevations in glucose.
Journal ArticleDOI

Nonsense mutation in the glucokinase gene causes early-onset non-insulin-dependent diabetes mellitus

TL;DR: The identification of a nonsense mutation in the gene encoding glucokinase and its linkage with early-onset diabetes in one family is reported, the first evidence implicating a mutation in a gene involved in glucose metabolism in the pathogenesis of NIDDM.
Journal ArticleDOI

Beta-cell lines derived from transgenic mice expressing a hybrid insulin gene-oncogene

TL;DR: Three pancreatic beta-cell lines established from insulinomas derived from transgenic mice carrying a hybrid insulin-promoted simian virus 40 tumor antigen gene can be used both to immortalize a rare cell type and to provide a selection for the maintenance of its differentiated phenotype.
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